"b^  O  \ 


in  tfje  Citp  of  i^eto  ^orfe 
?cf)ool  of  Bental  anb  (J^ral  burger? 


J^eference  i^ifararp 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

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http://www.archive.org/details/textbookofdental1908burc 


A  TEXT-BOOK 

OF 

DENTAL  PATHOLOGY 

AND 

THERAPEUTICS 

FOR  STUDENTS  AND  PRACTITIONERS 


BASED    UPON    THE    ORIGINAL    OF 


HENRY  H.  BURCHAKD,  M.D.,  D.D.S. 

LATE   SPECIAL   LECTURER   ON    DENTAL    PATHOLOGY    AND   THERAPEUTICS    IN   THE    PHILADELPHIA 

DENTAL   COLLEGE 


REWRITTEN  BY 

OTTO  E.  INGLIS,  D.U.S. 

PROFESSOR    OF   DENTAL   PATHOLOGY   AND  THERAPEUTICS   IN  THE    PHILADELPHIA 
DENTAL   COLLEGE 


THIRD  EDITION,  THOROUGHLY  REVISED 
ILLUSTRATED  WITH   567  ENGRAVINGS  AND  A  COLORED    PLATE 


LEA   &   FEBIGER 

PHILADELPHIA    AND    NEW    YORK 

1908 


Entered  according  to  the  Act  of  Congress,  in  the  year  1908,  bj- 

LEA    &    FEBIGER 
in  the  Office  of  the  Librarian  of  Congress.     All  rights  reserved. 


THIS 


VOLUME 


IS  RESPECTFULLY  DEDICATED 


RUSSELL  H.  CONWELL,  D.D.,  LL.D. 


IN  RECOGNITION  OF  HIS  UNSELFISH 


EFFORTS  IN  THE 


OPENING  OF  OPPORTUNITIES 


FOR  EDUCATION 


PREFACE  TO  THIRD  EDITION. 


As  ill  the  second  edition,  the  Editor  has  endeavored  to  maintain 
the  original  idea  of  a  text-book  furnishing  a  description  of  each  dental 
disease  and  its  treatment  in  such  manner  that  teachers  may  find  it 
a  useful  adjunct  in  the  presentation  of  dental  pathology  and  thera- 
peutics to  their  students.  The  flevelopment  in  this  branch  of  dental 
science  during  the  last  few  years  has  necessitated  many  changes  in 
the  text  to  reflect  the  present  advanced  position  of  the  entire  subject. 
Many  new  illustrations  have  been  added  to  increase  its  value  for 
didactic  purposes. 

The  thanks  of  the  Editor  are  due  to  those  who  have  kindly  loaned 
valuable  illustrations.     In  no  instance  has  a  request  been  denied. 

The  Editor  also  takes  this  opportunity  to  express  his  warm  appre- 
ciation of  the  continued  favor  bestowed  on  this  work  by  professors  and 
teachers  of  the  subject  throughout  this  Continent. 

O.  E.  I. 

Philadelphia,  1908. 


PREFACE  TO  FIRST  EDITION. 


This  volume  is  designed  as  a  text-book  of  the  principles  and  prac- 
tice of  dental  medicine  for  the  use  of  students,  and  as  a  reference  work 
on  applied  special  pathology  and  therapeutics  for  the  use  of  dentists. 
Accepting  the  dictum  of  the  advanced  teachers  of  the  day,  the  writer 
believes  that  an  entirely  rational  system  of  dental  medicine  can  have 
but  one  basis — namely,  the  same  principles  which  underlie  general 
medical  and  surgical  practice.  The  book  represents,  therefore,  an 
attempt  at  formulating,  from  data  obtained  from  every  available 
source,  a  system  of  dental  pathology  and  therapeutics  of  which  the 
several  parts  shall  be  in  harmony  with  one  another  and  also  with  the 
several  collateral  sciences  involved.  The  impulse  prompting  the  work 
was  no  desire  to  multiply  books,  but  arose  from  a  conviction  expressed 
by  many  teachers,  that  such  a  volume  is  needed  by  students,  prac- 
titioners, and  teachers. 

The  extent  and  scope  of  references  may  be  only  partially  seen  in 
the  numerous  foot-note  references,  space  limitations  precluding  any 
exhaustive  bibliography. 

It  would  be  unjust,  however,  to  omit  this  opportunity  to  credit 
two  investigators  without  whose  researches  this  volume  would  have 
been  impossible:  Professors  G.  V.  Black  and  W.  D.  Miller,  to  whom 
frequent  and  specific  references  are  made. 

The  innnense  development  of  modern  dentistry  has  brought  witii 
it  a  more  rational  and  convenient  grouping  of  its  subjects.  The 
American  Text-books  of  Operative  and  Prosthetic  Dentistry  have 
already  won  acceptance,  each  in  its  own  field.  They  leave  untouched 
a  range  of  subjects  which  are  naturally  cognate,  and  hence  are  most 
advantageously  taught  in  conjunction — namely.  Dental  Pathology, 
Therapeutics,  and  Pharmacology.  The  fitness  of  tliis  grouping  is 
manifest. 

H.  H.  B. 


v 


CONTENTS. 

SECTION    I. 

GENERAL  PATHOLOGY. 

CHAPTER  I. 

General  Principles 17 

CHAPTER  II. 

Causes  of  Disease,  General  and  Local 27 

CHAPTER  III. 
Mxcro6rg.\nisms  as  Exciting  Causes  of  Disease        ...  35 

CHAPTER  TV. 

Disturbances  of  Nutrition 59 

CHAPTER  V. 

Disturb.^nces  of  the  Vascular  System 105 

SECTION   IL 
EMBRYOLOGY,  ANATOMi^  AND  HISTOLOGY. 

CHAPTER  VI. 

The  Develop.ment,  Anato.my,  and  Hi.stology  of  the  Jaws  and  Teeth     145 

CHAPTER  VII. 

The  First  and  Second  Dentition.s;  Their  Progress,  Vari.\tions,  and 

Attendant  Disorders  ISl 

CHAPTER  VIII. 
M.a.lform.^tioxs  and  .Malpo.-^itions  of  the  Teeth 222 


X 


CONTENTS 


SECTION    III. 
AFFECTIONS  OF  THE  ENAMEL  AND  DENTINE. 

CHAPTER  IX. 

Abrasions,  Erosions,  and  Mechanical  Injury  op  the  Teeth       .      .     269 

CHAPTER  X. 
Stains  of  the  Enamel  and  Dentine 296 

CHAPTER  XI. 

Dental  Caries:  History;  Exciting  and  Predisposing  Causes       .      .     304 

CHAPTER  XII. 
Dental  Caries  :  Pathology,  Morbid  Anatomy,  and  Clinical  History        323 

CHAPTER  XIII. 

Dental  Caries:   Diagnosis,  Symptoms,  and  Prognosis.     Hypersensi- 
tivity OF  Dentine         -^'^^ 

CHAPTER  XIV. 
Dental  Caries:  Therapeutics  and  Prophylaxis 374 


SECTION    IV. 

DISEASES  OF  THE  DENTAL  PULP. 

CHAPTER  XV. 
Constructive  Diseases ^^•*- 

CHAPTER  XVI. 
Destructive  Diseases  of  the  Dental  Pulp 422 

CHAPTER  XVII. 

Methods  of  Removal  of  the  Dental  Pulp  and  Root-canal  Filling     .     466 

CHAPTER  XVIII. 

Gangrene  of  the  Pulp       


CONTENTS  XI 

SECTION   V. 
DISEASES  OF  THE  PERICEMENTUM. 

CHAPTER  XIX. 
Septic  Apical  Pericementitis  (Acute) 515 

CHAPTER  XX. 

Chronic  Septic,  Purulent,  Apical  Pericementitis   (Chronic  Apical 

Abscess) '^'^^ 


CHAPTER  XXI. 


Non-septic  Pericementitis 


563 


SECTION    VI. 

PERICEMENTAL  DISEASES   BEGINNING  AT  THE 
GUM  MARGIN. 


CHAPTER  XXII. 


Gingivitis    . 


591 


CHAPTER  XXIII. 

Salivary  and  Serumal  Calculus 606 

CHAPTER  XXIV. 

P-iORRHEA   AlVEOLARIS ^'— '' 

CHAPTER  XXV. 
Pericemental  Abscess "^' 

CHAPTER  XXVI 
Reflex  Disorders  of  Dental  Origin G66 

CHAPTER  XXVII. 
Infections  of  and  from  the  Mouth,  and  .Sterilization     ....     6S0 


DENTAL  PATHOLOGY  AND  THERAPEUTICS. 


SECTION  L 

GENERAL  PATHOLOGY. 


CHAPTER    I. 
GENERAL  PRINCIPLES. 

General  pathology  (pathos,  disease,  and  logos,  a  discourse)  is  that 
branch  of  science  which  treats  of  the  modifications  in  function  and 
changes  in  structure  occurring  in  disease.  It  embraces  all  pathological 
processes  occurring  in  the  human  body,  and  as  many  of  these  occur 
in  and  about  the  teeth  modified  only  by  the  peculiar  anatomy  of  the 
parts,  Dental  Pathology  may  be  said  to  be  that  branch  of  dental 
science  which  treats  of  modifications  in  fiuiction  and  changes  in 
structure  occurring  in  the  diseases  of  the  teeth  and  associate  parts. 

This  being  true,  it  follows  that  the  study  of  dental  pathology  nuist 
be  preceded  by  a  study  of  the  general  disease  processes  which  aifect 
the  tissues  of  the  body,  and  such  of  these  as  are  applicable  to  the  study 
are  known  as  the  General  Principles. 

The  word  Therapeutics  is  derived  from  the  Greek  thcrapcuin,  to 
take  care  of,  meaning  the  measures  adopted  to  remedy  or  remove 
the  changes  induced  by  pathological  processes. 

The  study  of  the  pathology  of  a  part  begins  with  a  study  of  its 
anatomy  and  histology,  then  naturally  follows  a  study  of  its  physiology 
and  embryology.  These  form  the  basis  from  which  degrees  of  abnor- 
mal function  and  altered  structure  may  be  judged  by  comparison 
with  similar  processes  occurring  in  other  j)arts  of  the  body. 

The  body  is  composed  of  cells  held  together  by  intercelhilar  sul)- 
stance.  These  cells  are  the  essential  functionatiiiir  parts  of  the  oriran- 
ism;  each  cell  is  composed  of  a  small  mass  of  protoplasm  containing 


18  GENERAL  PATHOLOGY 

in  nearly  all  cases  a  nucleus,  and  has  a  form  adapted  to  its  environ- 
ment and  function.  The  exact  chemical  composition  of  protoplasm 
is  unkno^^^l  and  efforts  at  analysis  destroy  its  peculiar  property  as  a 
substance  exhibiting  a  sequence  of  phenomena  called  life.  It  is  a  viscid 
substance  composed  physically  of  a  network,  the  spongioplasm,  con- 
taining a  slightly  more  fluid  substance,  the  hyaloplasm.^  Chemically 
it  is  70  per  cent,  water  containing  a  collection  of  proteids  and  differs 
as  to  these  in  the  different  classes  of  cells.  Proteids  are  but  imperfectly 
understood,  but  are  kno^Mi  to  consist  essentially  of  carbon,  hydrogen, 
oxygen,  and  nitrogen,  combined  with  sulphur  and  other  var3dng 
elements  in  enormous  molecules  approximately  represented  by  the 
formula  C4ooH3ioOi2oN5oS.^  This  formula  represents  merely  the  quan- 
tities of  these  elements  which  are  probably  combined  into  various 
chemical  compounds  in  the  cell,  including  one  or  more  carbohydrate 
radicals,  and  each  having  its  peculiar  affinity  for  food  materials. 


Changes  of  form  in  an  ameba:  PP,  pseudopodia;   V ,  vesicle;  N,  nucleus. 

capacity  for  energy  or  function,  and  reduction  of  waste  or  useless  cell 
material.  The  study  of  the  properties  of  cell  protoplasm  may  be  made 
by  observing  in  situ  the  action  of  living  cells  under  normal  conditions 
and  when  subjected  to  artificial  stimuli,  and  by  observing  the  action  of 
free  single  cells  such  as  an  ameba  under  like  conditions. 

If  a  drop  of  water  be  taken  from  the  sides  or  bottom  of  an  aquarium, 
placed  on  a  slide  and  covered  with  a  cover-glass,  and  then  placed  under 
a  microscope  with,  first,  a  ^  objective,  there  will  be  noted  at  some 
portion  of  the  fluid  a  small  transparent  mass  having  the  appearance 
of  a  colorless  fragment  of  jelly;  this  is  an  ameba.  The  outline  of  the 
mass  may  have  almost  any  form.  At  some  portion  there  will  be  a 
defined  and  easily  distinguished  spot,  the  nucleus;  at  another  point  a 
vesicle  is  seen;  the  body  of  the  ameba  appears  to  contain  numbers  of 
fine  granules.     The  nucleus  appears  more  markedly  granular  than 

'  Kirkos'  Pliysiology.  '  Schofield,  Elementary  Physiology. 


GENERAL  PRINCIPLES  19 

the  body  of  the  ameba.  If  kept  under  observation,  the  anieha  will  be 
seen  to  change  its  outlines;  at  one  or  more,  and  it  may  be  in  several 
places,  projections  like  blunt  arms  or  feet  are  seen  to  be  extending 
from  the  ameba  (Fig.  1),  On  account  of  their  appearance  they  are 
called  by  the  physiologist  pseudopodia,  from  pseudo,  false,  and  pons, 
a  foot — false  feet.    These  changes  of  form  are  much  varied  (Fig.  2). 

Fig.  2 


Ameboid  mi)\ement  of  a  white  blood  corpuscle  of  man;   various  phases  of  movement.      (Klein.) 

The  cell  has,  therefore,  the  property  of  altering  its  form — i.  e.,  it  has 
contractility.  If  the  temperature  of  the  slide  be  raised  the  movements 
of  the  cell  become  more  rapid,  and  if  raised  to  a  temperature  of  55°  C. 
the  cell  contracts  in  a  round  lump;  it  responds  to  stimuli,  and  has 
therefore  the  property  of  irritability. 

When  certain  solid  substances  contained  in  the  water  come  in  con- 
tact with  the  ameba,  the  latter  is  seen  to  flow  around  and  engulf 
them;  as  is  shown  in  Figs.  3  and  4,  where  the  analogue  of  an  ameba, 
a  leukocyte,  has  taken  in  bacteria  (phagocytosis).  After  a  time  the 
ingested  body  is  found  to  have  disappeared;  it  has  been  digested. 
Evidently  the  cell  must  produce  a  substance  capable  of  dissolving 

Fig.  3  Fig.   4 


Fig.  3. — Leukocyte  of  a  frog  from  the  neighborhood  of  a  piece  of  the  lung  of  a  mouse  infected 
with  anthrax,  about  forty-two  hours  after  the  piece  of  lung  had  been  placed  under  the  skin  of 
the  frog's  back.  The  leukocyte  is  in  the  act  of  eating  up  an  anthrax  bacillus.  (Brunton,  after 
Metchnikoff.) 

Fig.  4.— The  same  leukocyte  a  few  minutes  later,  after  it  has  completely  enveloped  the 
bacillus.     (Brunton,  after  MetchnikofT.) 

some  foreign  substances — i.  c,  it  has  the  function  of  secretion.  This 
is  probably  due  to  a  digestive  enzyme  analogous  to  pepsin.  ^Nlore 
than  this,  the  ameba  does  not  take  in  substances  indiscriminately; 
some  it  rejects. 

If  the  observations  are  continued,  it  will  be  noticed  that  changes 
occur  in  the  nucleus  of  the  cell.  A  series  of  alterations  in  its  fiffure 
are  noted,  as  shown  in  Fig.  5.  Two  nuclei  are  formed,  and  soon  the 
body  of  the  cell  divides  and  two  cells  appear — the  ameba  has  repro- 


20 


GENERAL  PATHOLOGY 


duced  itself.  This  primitive  cell  has,  therefore,  the  properties  of  irrita- 
bility, contractility,  secretion  and  excretion  (as  will  be  seen  in  later 
studies),  and  reproduction;  moreover,  it  responds  to  stimuli,  as  seen 
on  warming  the  stage. 

If  the  stage  be  cooled,  the  movements  of  the  protoplasm  are  less- 
ened, and  w^hen  foreign  substances  come  in  contact  with  the  cell  it 
fails  to  encompass  them — its  irritability  and  contractility  are  lessened. 

It  is  noted  that  some  simple  cells  are  attracted  and  stimulated  by 
light;  others  are  repelled  by  it. 

If  a  mild  induction  (interrupted)  current  be  passed  through  the 
water  in  which  the  ameba  is,  the  movements  of  the  cells  are  checked; 
if  a  strong  current  be  passed,  the  cell  contracts  sharply.    If  a  galvanic 

Fig.  5 


Forms  assumed  by  a  nucleus  in  dividing:  a,  resting  nucleus;  h,  skein-form,  open  stage;  c, 
wreath-form;  rf,  aster,  or  star-form;  e,  equatorial  stage  of  division;  /,  separation  more  advanced; 
g  and  h,  star  and  wreath  forms  of  daughter-nuclei.  (Reduced  from  Flemming's  drawings  in  the 
Arch.  f.  Mik.  Anat.) 

(constant)  current  be  passed,  movement  at  first  ceases,  but  pseudo- 
podia  are  extruded  toward  the  cathode  and  the  cell  crawls  toward 
that  pole.^ 

The  cell  responds  to  mechanical  stimuli,  such  as  violent  shaking, 
by  contraction.^ 

If  substances  such  as  ether  or  chloroform  are  added  to  the  fluid,  the 
irritability  of  the  cell  is  so  lessened  that  it  does  not  respond  to  stimuli. 

If  the  supply  of  oxygen  be  cut  off,  or  if  carbon  dioxide  be  admitted 
to  the  fluid,  movement  ceases  and  the  cell  remains  contracted. 

These  examples  serve  to  illustrate  that  protoplasm  responds  to 
stimuli  of  physical  and  chemical  nature,  and  that  its  functions  may  be 
altered  by  substances  which  are  brought  in  contact  with  it.  Upon 
these  facts  depends  the  practice  of  therapeutics. 


»  O.  Hertwig,  The  Cell. 


2  Ibid 


GENERAL  PRINCIPLES  21 

A  living  organism,  it  will  be  seen,  has  a  certain  degree  of  action 
and  function.  The  general  average  of  its  action  and  function  is  spoken 
of  as  a  condition  of  heaUii.  When,  from  any  cause,  the  functions  are 
raised  or  lowered  from  the  general  average,  a  condition  of  disease 
exists. 

Stimulation. — Certain  agencies  applied  to  the  cell  increase  its 
activity;  this  is  called  stimulation.  The  movements  of  the  cell  become 
more  rapid,  food  particles  are  taken  in  more  rapidly  and  disappear 
more  quickly;  irritability,  contractility,  and  secretion  are  increased. 
The  cell  subdivides,  or  reproduces  more  cjuickly.  Increase  the  stimu- 
lation, and  the  vital  activity  becomes  fretful;  in  some  cases  cell  divi- 
sion is  incomplete — the  nucleus  divides,  but  not  the  cell  body.  Increase 
the  stimulation  beyond  this  degree,  and  the  wearied  cell  ceases  its 
movements — refuses  to  respond;  is  paralyzed  by  overwork. 

Sedation.— If  the  conditions  be  reversed;  if,  instead  of  ap])lying  a 
stimulus  to  the  cell,  an  opposite  influence  be  introduced,  the  phe- 
nomena are  reversed. 

If  the  temperature  be  reduced,  the  movements  of  the  cell  become 
sluggish;  the  body  changes  its  form  more  sk)wly  and  less  extensively — 
i.  e.,  contractility  is  lessened;  particles  taken  into  the  cell  remain 
apparently  unchanged;  irritability,  secretion,  and  excretion  are  less- 
ened; and,  furthermore,  reproduction  does  not  occur  nearly  so  rapidly 
— that  is,  the  cell  hi  contact  with  sedative  influences  has  all  of  its 
activities  lessened. 

There  are  two  great  classes  of  influences,  then,  which  affect  the 
vitality  of  cells:  stimulation,  which,  if  continued  long  enough,  leads 
to  death  through  overwork;  and  sedation,  which,  if  continued,  para- 
lyzes all  of  the  energies  of  the  cell — it  is  starved  to  death. 

Every  cell  has  a  range  of  resistance  to  these  influences  which  tend 
to  destroy  it,  which  is  fitly  termed  the  resistance  of  vitality.  Disease 
itself  is  some  alteration  in  any  one  or  more  of  these  several  cell  proper- 
ties, of  irritaliility,  contractility,  growth,  secretion,  maintenance,  or 
reproduction.  If  any  one  of  these  jiroperties  is  not  exhibited,  it  is 
said  that  the  cell  is  diseased. 

If  a  brood  of  cells  derived  from  one  parent  be  examined,  some  will 
be  seen  to  grow  more  rapidly  than  others,  their  movements  are  more 
rapid  and  they  reproduce  more  tjuickly;  others  have  sluggish  func- 
tions and  movements. 

The  cell  lives  its  cycle  and  reproduces,  and  the  parent  is  no  more, 
the  life  being  continued  in  the  ofl'spring. 


22  GENERAL  PATHOLOGY 

The  life  and  properties  of  this  small  mass  of  protoplasm  represent 
in  miniature  the  primitive  fmictions  and  life  of  the  highest  animals. 

The  contractility  is  represented  in  the  motive  apparatus  of  the  higher 
animals. 

The  reception,  engulfing,  and  dissolving,  or  casting  out,  bodies  with 
which  the  ameba  is  brought  in  contact  correspond  in  the  higher  animals 
with  the  digestive  apparatus  and  process  and  the  excretory  function. 

The  highly  evolved  irritability  is  represented  in  the  nervous  system 
of  the  higher  animals. 

The  movements  occurring  in  and  about  the  vacuole  are  the  pro- 
genitors of  the  circulatory  apparatus  and  all  of  its  adjunct  organs. 

If  the  irritability  of  a  simple  cell  be  increased  or  diminished,  it 
corresponds  with  a  disease  of  the  nervous  system,  and  so  with  the 
other  functions. 

In  the  human  body  certain  collections  of  cells  are  found  in  which  one 
function  is  active,  the  others  in  abeyance;  thus,  large  colonies  of  cells 
exist  in  which  contractility  is  the  dominant  property  noted;  these  are 
muscle  cells.  Others  have  but  the  property  of  irritability;  these  are 
nerve  cells.  Still  others  develop  peculiar  chemical  functions,  and 
become  glandular  or  secretory  cells.  Such  collections  of  cells  are 
known  as  tissues.  These  special  cell  colonies  or  tissues  are  built 
together  into  defined  masses  for  the  performance  of  their  specialized 
functions.  Li  the  development  of  these  masses,  means  of  holding  and 
maintaining  the  cells  in  definite  mass  forms  and  provisions  for  their 
food  supply  and  waste-removing  apparatus  are  provided  in  what  are 
called  the  connective  tissues,  binding  the  cells  in  definite  forms  and 
transmitting  their  vascular  supply  (food-  and  waste-carrier).  When 
thus  bound  together  the  tissues  are  said  to  form  organs. 

\Vhile  all  tissues  are  capable  of  analysis  into  cells  and  intercellular 
substance,  a  more  practical  view  may  resolve  the  tissues  into  (1)  func- 
tional cells;  (2)  a  supporting  intercellular  substance;  (3)  intercellular 
spaces  in  which  flows  the  lymph  derived  from  the  blood ;  (4)  the  chan- 
nels of  circulation  and  conductors  of  nervous  impulses — i.  e.,  arteries, 
capillaries,  veins,  lymphatics,  and  nerves.  The  arteries  bring  to  the 
tissues  the  blood  freighted  with  oxygen  and  nutrient  material.  As  it 
passes  through  the  capillaries  a  portion  of  the  blood  plasma,  under 
arterial  pressure  and  osmotic  force,  passes  into  the  intercellular  spaces 
into  contact  with  the  cells.    This  exuded  fluid  is  now  called  lymph. 

Stated  in  general  terms  the  food  materials  contained  in  arterial 
blood  and  furnished  to  the  tissues  by  way  of  the  lymph  are:  water, 


GENERAL  PRINCIPLES  23 

proteids,  glucose  and  fats  or  their  elements, inorganic  salts,  and  oxygen. 
From  this  store  the  cells  take  what  they  require,  and  within  themselves 
they  elaborate  substances  essential  to  their  growth  and  maintenance  as 
masses  of  functionating  protoplasm,  and  as  the  protoplasm  is  of  more 
complex  composition  than  the  majority  of  food  elements,  they  are  said 
to  form  from  simple  compounds  substances  of  a  higher  degree  of  com- 
plexity (anabolism).  From  their  substance  the  cells  eject  into  the 
lymph  stream  such  waste  products  as  result  from  the  breaking  down 
of  the  previously  formed  protoplasm  (catabolism). 

While  the  exact  nature  of  the  chemical  change  occurring  in  cells  is 
not  known,  the  present  thought  is  that  much  of  the  process  of  cell  met- 
abolism is  conducted  within  the  cell  through  the  action  of  one  or  more 
enzymes  which  have  the  power  of  catalytically  affecting  prompt  and 
smooth  chemical  changes  at  low  temperature  which  can  at  times  be 
produced  in  the  laboratory  only  by  experiments  not  at  all  comparable 
with  the  action  of  cells. 

Various  organs  of  the  body  evidently  prepare  the  food  material 
absorbed  by  the  intestines  for  the  use  of  the  cells — for  example,  gly- 
cogen is  formed  from  the  absorbed  glucose  by  the  ferment  of  liver 
cells,  and  when  needed  again  transformed  into  glucose. 

Ehrlich's  lateral  chain  theory  for  immunity  (which  see)  presupposes 
the  presence  of  atom  groups  of  protoplasm  surrounding  a  complex 
group  of  atom  groups,  the  nucleus,  each  atom  group  having  affinity 
for  a  particular  form  of  substance  presented  to  it.  These  he  terms 
receptors,  and  each  is  supposed  to  possess  a  combining  or  prehending 
group  of  atoms  called  an  haptophorous  group  and  a  ferment  group 
capable  of  altering  the  chemistry  of  the  food  element  to  suit  its  needs 
or  that  of  the  cell  as  a  whole;  this  latter  group  is  termed  a  zymoph- 
orous  group.  The  carbohydrates  and  fats  are  in  the  main  the  pro- 
ducers of  energy  and  are,  lastly,  resolved  into  glucose  and  fat  or  their 
elements  for  the  consumption  of  the  cells,  and  by  them  appropriated 
into  their  protoplasm,  whence,  by  catabolic  changes,  they  are  started 
upon  their  retrogressive  course  to  the  final  products  CO^  and  water. 
The  proteids  are  mainly  useful  for  the  building  of  the  cell  protoplasm 
and  its  maintenance,  and  when  catabolized  end  in  products  which 
in  other  organs  are  transformed  into  urea  and  uric  acid.  Experi- 
mental evidence  has  shown  that  after  energy  has  l)een  liberated  to  the 
point  of  fatigue,  there  is  an  actual  loss  of  substance  by  the  cells,  in 
consequence  of  which  they  become  smaller  and  of  different  histological 
appearance. 


24  GENERAL  PATHOLOGY 

It  is  evident,  therefore,  that  any  condition  which  will  produce  an 
expenditure  of  energy  without  a  compensating  restoration  of  cell 
material  must  result  in  a  malnutritional  process. 

There  is  evidence  that  changes  occur  in  the  cell  waste  either  in  the 
blood  or  in  various  organs  of  the  body.  While,  then,  the  bodily  ejecta 
contain  substances  fairly  constant  in  composition,  they  are  held  to 
represent  elaborations  of  cell  waste  rather  than  actual  cell  ejecta. 
For  example,  urea  is  pretty  certainly  derived  from  muscular  tissue, 
yet  is  nearly  absent  in  muscle  and  is  supposed  to  be  due  to  the  dehy- 
dration of  ammonium  carbonate  in  the  liver. ^  Lactic  acid  and  ammo- 
nium carbonate  have  been  experimentally  shown  to  be  probably  com- 
bined into  uric  acid  in  the  liver.  The  cell  waste  is  carried  by  the 
lymph  into  the  lymphatics  connecting  with  the  intercellular  spaces. 
Thence  it  is  delivered  by  way  of  the  venous  system  to  the  circulation 
for  further  elaboration  and  elimination  from  the  body.  Any  inter- 
ference with  such  elaboration  or  elimination  must  of  necessity  result 
in  a  retention  of  waste  products  within  the  system,  probably  leading 
to  irritation  and  disturbance  of  metabolism  in  all  cells. 

Cell  metabolism  is  a  chemical  change  and  is  therefore  accompanied 
by  heat  production.  Energy  is  stored  up  in  the  cell  as  latent  force 
capable  of  liberation  under  stimulus,  which  force  is  expressed  in 
various  forms  of  functional  activity — i.  e.,  contractility  in  muscular 
tissue,  irritability  and  mentality  in  nervous  tissue,  secretion  in  the 
various  secretory  glands,  eliminative  selection  in  the  various  excretory 
organs,  etc.  Cells  after  a  period  of  activity  undergo  degenerative  pro- 
cesses, and  are  removed  or  reproduced  by  the  process  of  mitosis  (Fig.  5). 

The  life  conditions  of  cells  are  necessarily  those  under  which  they 
best  perform  these  functions  without  exhaustion,  and  are  the  follow- 
ing: (1)  A  proper  food  supply,  including  water  and  oxygen;  (2) 
a  proper  temperature;  (3)  a  proper  removal  of  waste  products; 
(4)'  possibly  a  proper  innervation.  Any  interference  with  these  con- 
ditions, which  may  be  termed  the  normal  physiological  conditions, 
results  in  a  morbid  process  of  physiology  or  pathological  physiology  or 
pathology  m  its  limited  sense.  With  such  interference  disease  may  be 
said  to  begin.  The  definition  of  disease  as  an  alteration  of  nutrition 
is  therefore  appropriate.  For  this  reason  the  proximate  exciting 
causes  of  disease  are  classed  as  (1)  abnormal  food  supply;  (2)  abnor- 
mal waste  removal;  (3)  abnormal  physical  condition;  (4)  abnormal 
nerve  supply. 

*  Kirkes'  Pliysiology. 


GENERAL  PRIXCIPLES  25 

The  niorbiVl  j)hysiology  results  in  morbid  products  or  in  retained 
normal  j)roducts  and  an  altered  cell  function.  When  pronounced 
this  is  spoken  of  as  Functional  Disease,  although  it  may  be  said  to 
be  in  existence  even  if  discomfort  be  not  produced.  Sooner  or  later 
an  abnormal  change  in  the  histological  characteristics  of  the  cells 
or  intercellular  substance  may  occur  which  has  been  referred  to  as 
Morbid  Histology  or  Pathological  Histology.  As  definite  microscopic 
and  often  macroscopic  appearances  are  associated  with  certain  dis- 
eased conditions,  these  are  referred  to  as  the  Morbid  Anatomy  of  a 
Disease  or  Pathological  Anatomy.  The  phenomena  associated  with  a 
disease  are  called  its  Semeiology  (semeion,  a  mark  or  sign)  or  Symp- 
tomatology, and  are  either  described  by  the  patient  as  sensations  or 
pains  of  varied  character  or  situation  (Subjective  Symptoms),  or  may 
be  noted  by  normal  or  aided  vision,  by  physical  examination,  or 
chemical  analvsis  (Objective  Symptoms).  That  which  excites  a 
disease  or  promotes  the  action  of  the  excitation  is  called  a  Disease 
Cause.  The  study  of  disease  causes  is  Etiolog}'  {aeiios,  a  cause,  and 
logos).  It  is  noted  that  diseases  having  a  fairly  defined  pathology  and 
morbid  anatomy  have  from  their  beginning  to  ending  tolerably  con- 
stant phenomena;  they  have  each  a  natural  history;  this  is  called  the 
Clinical  History  of  a  Disease. 

The  study  of  the  origin  and  development  of  a  disease  together  is 
known  as  its  Pathogenesis  (pathos,  disease;  gennao,  I  produce). 
Through  the  study  of  the  characteristic  symptoms  of  diseases,  as  well 
as  those  common  to  several  diseases,  a  particular  disease  may  be 
distinguished.  This  is  called  Diagnosis  {dia,  through;  gignosko,  I 
know) — Direct  Diagnosis  when  there  is  no  question  as  to  the  symp- 
toms, Difi'erential  Diagnosis  when  several  diseases  are  possible  and 
the  characteristics  of  one  are  considered  as  more  pronoiniced.  Under 
certain  circumstances  a  disease  may  be  inferred  to  be  present  by 
excluding  all  other  possible  conditions  (Diagnosis  by  Exclusion).  In 
the  coiu'se  of  a  disease  experience  has  shown  that  certain  signs  and 
symptoms  are  apt  to  be  followed  by  good  or  ill  results,  as  the  case  may 
be.  By  these  signs  and  symptoms  it  may  be  foretold  with  some  degree 
of  assurance  what  will  be  the  probable  outcome  of  the  disease.  The 
inference  based  upon  these  symptoms  is  known  as  the  Prognosis 
{pro,  before,  and  gignosko,  I  know).  The  care  of  or  treatment  of  a 
disease  is  its  Therapeutics.  This  involves  a  knowledge  of  remedies 
applicable,  known  as  the  Materia  Medica.  When  applieil  upon  the 
basis  of  a  scientific  study  of  the  pathogenesis,  clinical  history,  and 


26  GENERAL  PATHOLOGY 

prognosis  of  disease  and  a  parallel  knowledge  of  the  physiological 
action  of  drugs  and  of  other  remedies,  the  treatment  is  known  as 
Rational  Therapeutics.  WTien  the  treatment  is  based  upon  the  known 
good  effects  of  a  remedy  in  a  certain  disease,  and  not  upon  its  physio- 
logical action,  it  is  known  as  Empirical  Therapeutics. 

The  pathogenesis  of  a  disease  being  known,  intelligent  efforts  may 
be  exerted  for  its  prevention.  The  causes  may  be  removed  or  neutral- 
ized before  they  have  an  opportunity  to  act;  this  is  Prophylaxis.  The 
science  of  prevention  of  disease  upon  the  broad  basis  of  a  knowledge 
of  and  observance  of  laws  of  health  is  Hygiene. 

It  will  be  seen  that  a  knowledge  of  special  pathology  can  only  be 
obtamed  from  (1)  a  knowledge  of  pathology  in  general  or  at  least  of 
those  principles  of  general  pathology  which  underlie  all  disease  pro- 
cesses; (2)  a  knowledge  of  the  local  anatomy  and  histology;  (3)  a 
knowledge  of  local  embryology  and  physiology;  (4)  a  study  of  local 
pathology  and  morbid  anatomy.  To  this  must  be  added  a  study  of 
materia  medica  and  special  therapeutics. 


CHAPTER    II. 
CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL. 

A  DISEASE  cause  may  be  defined  as  any  influence  of  whatsoever 
nature  which  is  capable  of  disturbing  the  nutritive  balance  of  any 
portion  of  the  body.  The  branch  of  study  which  deals  with  the  causes 
of  disease  is  called  Etiology. 

The  causes  of  disease  are  classed  as  Exciting  (or  Determining)  and 
Predisposing.  These  are  each  divisible  into  Extrinsic,  originating 
from  without,  and  Intrinsic,  originating  within  the  body. 

EXCITING  CAUSES  OF  DISEASE. 

These  are  influences,  either  extrinsic  or  intrinsic,  which  are  com- 
petent to  suddenly  or  gradually  interfere  with  the  nutrition  of  the  cells 
of  a  part  or  with  the  general  nutrition  of  cells.  These  influences  are 
very  numerous,  but  may  be  grouped  according  to  their  action  under  a 
few  convenient  headings:  (1)  Abnormal  Food  Supply.  (2)  Abnor- 
mal Waste  Removal.  (3)  Abnormal  Physical  Conditions.  (4) 
Abnormal  Nerve  Supply. 

These  are  termed  the  Proximate  Exciting  Causes,  as  their  efl^ects 
are  immediately  exerted  upon  the  cells.    Other  causes  may  be  back 
of  these  and  are  spoken  of  as  Primary  (or  Contributory)  Causes— ^.  g., 
tuberculosis  of  the  lungs  (primary)  may  cause  insufficient  oxygenation 
of  the  blood  which  constitutes  an  abnormal  food  supply  (proximate). 
Abnormal  Food  Supply.— By  abnormal  food  supply  is  meant  an 
altered  (juantity  or  ([uality  of  nutritive  elements  delivered  to  the  cells 
either  of  a  part  or  of  the  entire  body.    The  primary  causes  of  this  may 
exist  as  disturbances  or  faults  in  any  of  the  food-elaborating  organs, 
the  lungs,  the  eliminating  organs,  or  the  oxygen  carriers  of  the  blood 
may  exist  in  lessened  numbers.    In  the  first  case  the  quality  or  quan- 
tity of  nutritive  material  is  impaired,  in  the  second  case  oxygenation 
is  insufficient,  and  in  the  third  case  material  injurious  to  cells  are 
retamed  in  the  body  and  are  again  presented  as  food  to  the  cells,  actmg 
as  poisons.    Poisonous  or  even  non-poisonous  drugs,  and  the  products 


28  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL 

of  bacterial  action,  whether  absorbed  from  the  intestines  or  from  foci 
of  infection,  have  all  more  or  less  deleterious  action  upon  cell  proto- 
plasm, violent  if  entering  the  blood  in  quantity,  chronic  if  entering 
continuously. 

Faults  in  the  circulatory  apparatus  interfering  with  the  circulation 
generally  cause  an  interference  with  general  nutrition,  while  local 
disturbances  of  the  circulation  from  any  cause  disturb  the  relations 
of  the  blood  supply  to  the  nutrition  of  a  part.  Thus,  the  fresh  blood 
supply  may  be  excessive,  as  in  the  milder  form  of  arterial  hyperemia, 
or  deficient,  as  in  venous  hyperemia  and  inflammation. 

Abnormal  Waste  Removal. — Abnormal  waste  removal  is  ordinarily 
included  under  the  heading  of  abnormal  food  supply,  and  it  is  evident 
that  retention  of  waste  in  the  blood  causes  the  presentation  to  cells 
of  an  abnormal  food  or  poison.  In  local  conditions,  such  as  venous 
hyperemia  and  inflammation,  the  stasis  causing  waste  retention  pre- 
vents the  access  of  a  fresh  food  supply  as  well.  In  kidney  disease 
the  substances  ordinarily  physiologically  eliminated  by  the  kidneys 
are  retained  in  the  blood  and  act  as  poisons  to  cell  protoplasm 
generally. 

Abnormal  Physical  Conditions. — ^This  class  of  disease  causes 
includes  all  injuries  due  to  any  of  the  physical  or  chemical  forces: 
Traumatic  injuries,  such  as  cuts,  bruises,  surgical  openings,  etc.: 
Mechanical  causes,  such  as  compressions,  obstructions  to  ducts  or 
the  natural  outlets  of  the  body,  faults  in  the  circulatory  mechanism, 
stoppages  in  the  arteries  or  veins:  Abnormal  temperature,  burns, 
freezing,  etc.:  Irritations  of  various  sorts,  such  as  those  due  to 
mustard,  arsenic,  etc.  Chemical  causes,  such  as  the  action  of  acids 
or  caustics,  and  the  local  effects  of  microorganisms  may  all  be  classi- 
fied under  this  heading.  The  disturbance  is  due  to  either  a  direct 
destruction  of  the  life  of  the  cells  or  an  interference  with  the  circula- 
tion in  a  part. 

Abnormal  Nerve  Supply. — It  is  known  that  division  of,  injury  to, 
or  disease  of  certain  nerves  causes  trophic  or  nutritional  changes  in 
the  part  to  which  they  are  supplied.  Whether  the  nutrition  of  the 
parts  is  controlled  by  special  trophic  nerve  fibers  has  not  been  demon- 
strated. Halliburton,^  in  support  of  the  trophic  influence  of  nerves, 
instances  that  wlien  the  fifth  nerve  (sensory)  is  divided  beyond  the 
Gasserian  ganglion,  ulceration  of  the  cornea  results;  while  if  the 
seventh  nerve  (motor)  be  divided  or  paralyzed,  the  eyeball  is  equally 

1  Kirkes'  Physiology. 


PREDISPOSING  CAUSES  OF  DISEASE  29 

exposed  to  irritants,  yet  does  not  ulcerate.  He  also  instances  that 
division  of  the  vagi  produces  fatty  degeneration  of  the  heart. 

While  admitting  the  lack  of  anatomical  proof,  he  regards  the  tro- 
phic influence  of  nerves  upon  parts  to  be  unexplainable  upon  the 
ground  taken  by  others,  that  all  apparently  trophic  changes  are  due 
to  distiu'bances  of  the  vasomotor  nerves  controlling  the  caliber  of 
vessels.  According  to  these  other  observers  degrees  of  dilatation  are 
produced  which  modify  the  amount  of  blood  delivered  to  a  part  and 
thus  modify  its  nutrition. 

Effects  are  produced  upon  nutrition  by  causes  which  can  act  onlv 
through  the  nervous  system — e.  g.,  the  eft'ect  of  anxiety  upon  appetite 
and  digestion.  The  interdependence  of  these  classes  of  causes  is 
almost  self-evident;  for  example,  constant  suppuration  at  a  focus  of 
infection  (abnormal  physical  condition)  may  induce  a  toxemia  (abnor- 
mal food  supply)  which  may  be  responsible  for  kidney  or  other  disease 
(abnormal  physical  condition),  resulting  in  the  retention  of  waste 
products  in  the  blood  (abnormal  waste  removal  or  food  supply),  which 
has  a  vicious  result  upon  all  metabolism,  including  that  of  the  nervous 
system,  inducing  in  tiu'n  an  abnormal  nerve  supply  and  lessening 
resistance  even  in  the  tissues  about  the  original  focus  of  infection. 
Such  a  train  of  events  is  known  as  the  establishment  of  a  vicious  circle. 


PREDISPOSING  CAUSES  OF  DISEASE. 

A  predisposing  cause  of  disease  is  one  which  influences  the  cells  or 
juices  of  the  body  or  part  in  such  a  manner  as  to  lessen  the  resistance 
to  the  action  of  the  exciting  causes  of  disease. 

It  must  be  considered  that  a  predisposition  or  lessened  resistance 
is  in  itself  a  condition  of  disease,  not  recognizalile,  perhaps,  yet  a  de- 
parture from  the  standard  of  the  best  health  of  an  individual  or  part. 
For  the  most  part  predisposition  is  regarded  in  its  relation  to  the 
extrinsic  causes  of  disease,  such  as  bacterial  influences.  In  such  a 
condition  the  individual  is  said  to  be  susceptible.  Predisposition  is 
either  general  or  local. 

General  Predisposition. — This  is  either  (1)  a  natural  or  inherent 
lack  of  resistance  (o  infectious  or  non-infectious  diseases,  or  (2)  an 
acquired  lack  of  resistance  to  infectious  or  non-infectious  diseases. 
The  human  race  in  general  is  naturally  predisposed  to  many  infectious 
diseases,  such  as  tuberculosis,  cholera,  malaria,  measles,  smallpox. 


30  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL 

typhoid  fever,  scarlet  fever,  and  syphilis/  When  a  person  is  exposed 
to  the  disease  and  contracts  it,  he  is  said  to  be  predisposed  to  it.  If  he 
does  not  contract  it,  his  system  is  immune  either  temporarily  or  per- 
manently. (See  Immunity.)  There  being  several  forms  of  immunity, 
the  lack  of  any  natural  form  may  be  considered  as  a  predisposition. 
This  immimity  is  ordinarily  operative  when  the  individual  is  in  the 
best  state  of  health,  and  v^^hen  a  departure  from  this  standard  is 
brought  about  by  any  cause,  exciting  infective  causes  may  then  act. 
This  is  acquired  predisposition.  Some  individuals  have  a  natural  or 
congenital  lessened  resistance  to  external  influences  of  a  non-infec- 
tious character,  such  as  heat  or  cold,  mental  effort,  or  nervous  irrita- 
tions of  a  degree  ordinarily  borne  by  the  great  majority  of  individuals. 
This  may  also  be  acquired,  as,  for  example,  by  extreme  subjection  to 
the  above  or  other  enervating  causes.  An  inherited  predisposition 
to  such  diseases  as  insanity,  cancer,  or  gout  may  exist. 

Some  persons  cannot  bear  certain  kinds  of  food  vi^ithout  illness,  or 
react  strongly  to  small  doses  of  drugs.  This  is  called  an  idiosyncrasy 
and  may  be  either  congenital  or  acquired. 

The  predisposing  causes  capable  of  producing  a  lessened  resist- 
ance may  be  grouped  under  a  few  headings. 

Sex  as  an  Intrinsic  Predisposing  Cause. — In  this  connection  the 
influence  of  sex  upon  predisposition  to  disease  must  be  considered. 
While  the  general  resistive  povi^er  of  the  bodies  of  both  sexes  may  be 
regarded  as  practically  equal  under  similar  conditions,  yet  the  anatom- 
ical structures  and  physiology  of  each  sex  have  an  influence  upon  pre- 
disposition to  certain  diseases.  Aside  from  the  diseases  peculiar  to  sex, 
on  account  of  their  peculiar  organs,  each  sex  exhibits  predispositions 
to  diseases  which  the  other  sex  escapes;  for  many  of  these  the  habits 
of  life  furnish  an  explanation,  for  others  an  explanation  is  not  avail- 
able. For  example,  while  women  are  predisposed  to  functional  and 
emotional  disturbances  of  the  nervous  system,  such  as  hysteria,  they 
are  almost  exempt  from  such  structural  nervous  diseases  as  locomotor 
ataxia  and  general  sclerosis.  Males  are  much  more  subject  to  hemo- 
philia than  women. 

Age. — During  the  first  two  years  after  birth  the  nervous  system 
and  the  appendages  of  the  alimentary  canal  are  developing,  and 
improper  feeding,  difficult  teething,  or  other  influences  readily  act 
as  exciting  causes  of  alimentary  or  nervous  disturbances. 

Later  children  are  subject  to  acute  infectious  diseases,  especially 
tuberculosis,  diphtheria,  and  the  eruptive  fevers.    At  adolescence  other 

1  Ziegler,  General  Pathology. 


PREDISPOSING  CAUSES  OF  DISEASE  31 

predispositions  occur,  notably  chlorosis  in  young  girls.  Later  come 
the  diseases  of  early  maturity,  such  as  typhoid  fever,  pulmonary' 
tuberculosis,  and  to  a  degree  dental  caries. 

In  old  age  or  middle  life  occur  arterial  and  other  degenerations 
and  diseases  consequent  upon  them  or  upon  overstimulation  of  organs 
or  tissues. 

Temperament. — ^Temperament  is  the  peculiar  congenital  consti- 
tution of  an  individual  imparting  certain  physical  characteristics  and 
certain  natural  tendencies.     There  are  four  basal  temperaments: 

The  sanguine  is  that  in  which  individuals  are  decidedly  inclined  to 
the  blonde  t}^e  with  evidence  of  an  abundance  of  the  nutritive  fluid,  the 
blood — i.  e.,  the  vascular  system  is  said  to  dominate  the  other  functions 
of  the  body.  Such  are  predisposed  to  acute  pulmonary  and  cardiac 
diseases  and  inflammatory  disturbances  of  serious  import.  The 
mental  characteristics  of  this  temperament  are  hopefuhiess,  cheerful- 
ness, and  solidity  but  floridity  of  mental  endowments.  The  recupera- 
tive power  is  good. 

The  bilious  temperament  is  characterized  by  a  decided  inclination  to 
the  brunette  type,  with  evidence  of  a  domination  of  other  functions  by 
the  liver.  There  is  a  tendency  to  hepatic  and  digestive  derangements 
and  despondency;  at  the  same  time  there  is  possessed  great  physical 
and  mental  strength,  together  with  a  reliable  recuperative  power. 

The  nervous  temperament  is  indicated  by  the  smallness  and  delicacy 
of  frame  and  the  quickness  of  motion  and  perception,  evidencing  a 
domination  by  the  nervous  system  to  diseases  of  which  such  tempera- 
ment predisposes. 

The  lymphatic  temperament  is  indicated  by  bulk,  pallor,  and  flac- 
cidity  of  tissue,  a  colorlessness  of  temperament,  indicating  an  inherent 
feebleness.  There  is  a  tendency  to  serious  chronic  conditions.  This 
temperament  is  accompanied  by  poor  recuperative  force. 

There  are  no  individuals  of  pure  basal  temperament,  so  that  the 
nearest  approach  is  a  dual  temperament,  such  as  the  biliosanguine, 
in  which  the  characteristics  of  the  sanguine  predominate  strongly 
modified  by  those  of  the  bilious  temperament.  In  like  manner  the 
sanguonervous,  nervolymphatic,  and  other  classes,  twelve  in  number, 
are  recognized  as  having  typical  representatives  in  each  community. 
A  third  or  ternary  classification  is  possible — e.  g.,  sanguonervo- 
bilious.  It  will  be  seen  that  temperament  has  a  distmct  relation  to 
the  vital  resistance  normally  implanted  in  an  individual,  and  there- 
fore may  to  a  certain  extent  be  counted  upon  in  a  prognosis.    Tem- 


32  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL 

perament  is  a  predisposing  cause  probably  only  in  so  far  as  it  intro- 
duces a  natural  general  lack  of  resistance  to  disease,  or  irresistibly 
drives  an  individual  into  certain  habits  of  life  which  may  become  the 
cause  of  a  lessened  resistance. 

Heredity. — Certain  diseases  exhibit  a  predisposition  to  descend 
from  parent  to  child  direct  or  from  grandparent  through  the  unaffected 
son  or  daughter  to  a  grandchild  (in  the  latter  case  it  is  called  atavistic 
hereditary  transmission,  also  remote  heredity). 

The  mode  of  transmission  is  m  all  probability  the  inheritance  of  a 
t\^e  of  tissue,  a  tissue  anatomy  and  physiology  v^^hich  permit  the 
more  ready  action  of  the  exciting  causes  of  the  disease.  This  tend- 
ency is  called  a  diathesis — e.  g.,  hemorrhagic  diathesis  (hemophilia), 
gouty  diathesis,  or  tuberculous  diathesis.  Diathesis  may  also  be 
acquired.  The  influence  of  race  may  also  be  considered  as  coming 
under  this  heading.     (See  Immunity.) 

Existing  Disease. — The  presence  of  one  disease  may  weaken  the 
resistance  of  a  part  or  the  organism  so  that  another  disease  may 
the  more  readily  become  implanted — e.  g.,  measles  followed  by 
pneumonia. 

Previous  Disease. — At  a  period  subsequent  to  disease  the  same 
disease  may  recur  or  another  disease  may  be  implanted — e.  g.,  pneu- 
monia predisposes  a  lung  to  a  recurrence  of  pneumonia,  or  tubercu- 
losis may  readily  follow.  Previous  disease  may  confer  immunity,  as, 
for  example,  in  smallpox  or  measles. 

Extrinsic  Predisposing  Causes  of  Disease. — Under  this  head  are  in- 
cluded all  those  conditions  of  external  origin  which  lessen  the  resist- 
ance of  an  individual  to  the  action  of  exciting  causes.  Excessive  heat 
is  weakening;  cold  and  dampness,  by  chilling  the  surface  of  the  body, 
cause  hyperemia  of  internal  parts  and  thus  predispose  to  such  diseases 
as  pneumonia,  rheumatism,  etc.  Fatigue,  unhealthy,  cramping,  or 
sedentary  occupations,  continued  loss  of  sleep  from  any  cause,  evil 
habits,  continued  hunger,  etc.,  are  other  examples  of  debilitating 
influences  which  may  be  partly  intrinsic. 

Local  Predisposition. — Alterations  in  the  normal  physiology  of 
a  part  are  apt  to  occur  through  certain  actions  upon  it,  thus  bring- 
ing it  into  a  condition  of  lessened  resistance,  permitting  the  action  of 
entirely  different  exciting  causes.  Apart  from  this  fact,  a  part  may 
be  predisposed,  by  nature  apparently,  to  permit  the  growth  of  organ- 
isms which  do  not  grow  well  in  other  tissues.  Local  depression  of 
tissue  vitality  predisposes  to  the  growth  of  organisms  in  the  tissues. 


IMMUNITY  33 

Thus  slight  injury  producing  either  arterial  or  venous  hyperemia  or 
ischemia  may  permit  bacteria  to  pnxhice  even  grave  consequences. 
More  severe  injury^  also  may  predispose,  but  the  contrary-  effect  has 
also  been  observed — i.  e.,  that  severe  injury  excites  a  phagocytic 
reaction  and  copious  exudation  of  lymph  (a  later  stage  of  inflamma- 
tion) which  antagonizes  the  bacteria.     (See  Inflammation.) 

The  structure  of  a  part  has  also  l)een  shown  to  have  an  effect  upon 
the  life  of  microorganisms  gaining  access  to  its  tissues.  The  tissues 
about  the  mouth  are  normally  notoriously  resistant  to  infections, 
but  at  times  are  exceedingly  susceptible,  as  in  pyorrhea  alveolaris. 
General  depression  of  vitality  also  necessarily  affects  the  resistive 
force  of  all  local  tissues.  Thus,  extensive  suppuration  is  more  liable 
to  occur  in  those  rendered  feeble  and  anemic  by  any  cause.  Ordinarily 
surgical  operations  about  the  mouth  were  successful  in  pre-aseptic 
times,  while  abdominal  or  g}aiecological  operations  were  attended  by 
an  enormous  percentage  of  death  from  infection. 

IMMUNITY. 

Immunity  is  the  opposite  of  predisposition  and,  like  it,  can  be  either 
natural  or  acquired.  It  signifies  an  insusceptibility  to  a  disease. 
Natural  immunity  to  a  particular  infectious  disease  can  only  be  deter- 
mined by  repeated  exposures,  and  may  then  fail  at  last  owing  to  some 
systemic  change.^  Immunity  may  be  exhibited  toward  only  one  dis- 
ease. In  some  persons  disease  appears  to  be  influenced  by  sex,  as, 
for  example,  males  have  a  general  immunity  from  goitre,  females 
from  Addison's  disease.  Immunity  is  influenced  by  age  in  certain 
diseases;  for  example,  the  diseases  of  childhood  are  rare  in  the  eklerly ; 
they  do  occur,  however.  The  degenerative  diseases  of  old  age  are 
almost  unknown  in  childhood.  Race  has  its  influence;  the  negro  is 
almost  immune  to  malaria  and  yellow  fever,  but  particularly  suscep- 
tible to  smallpox  and  tuberculosis.  The  natural  immunity  may  be 
more  apparent  than  real,  owing  to  failure  of  the  bacteria  to  find  a  local 
condition  favorable  to  development  and  to  enter  the  blood.  If  special 
care  in  experiment  be  taken  to  introduce  the  bacteria,  and  failure 
of  inoculation  result,  the  natural  immunity  is  absolute.  Example: 
Rats  to  diphtheria,  or  negroes  to  yellow  fever. 

A  striking  example  of  lost  immunity  occurred  in  the  case  of  a  friend, 
who,  in  early  and  middle  life,  could  handle  poison  ivy  with  impunity. 

'  Green,  Patliol<iKy  ami  Morhiil  Anatomy. 


34  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL 

On  approaching  seventy  years  of  age,  and  while  in  a  condition  of 
general  debility,  he  was  affected  from  head  to  foot  with  the  peculiar 
dermatitis  as  the  result  of  pulling  up  a  plant. 

The  further  discussion  of  immunity  as  related  to  bacterial  infection 
should  properly  be  discussed  after  the  consideration  of  bacterial 
causes,  and  will  be  found  at  the  end  of  Chapter  III. 


CHAPTER    III. 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 


The  infectious  and  contagious  diseases  have  for  the  most  part  been 
shown  to  be  caused  by  low  forms  of  vegetable  organisms  known  col- 
lectively as  fungi,  while  in  a  few  diseases  minute  animal  organisms 
(protozoa)  are  the  causes. 

The  following  table  shows  the  position  of  the  vegetable  organisms 
in  the  scale  of  vegetable  life  and  gives  the  lowest  forms  of  animal  life : 

f  Phanerogams:  plants  reproducing  by  flowers  and  seeds. 


Vegetable     ,  Cryptogams, 
kingdom      reproducing 
by  spore 
formation  or 
.    division. 


Leafy  cryptogams. 
Thallophytes, 
having  no 
"I        distinction 
between  the 
leaf  and  stem. 


Lichens. 
i-  Algie. 
Fungi. 


Schizomycetes 
(fission  fungi). 

Hjrphomycetes 
(mould  fungi). 

Blastomycetes 
(bud  fungi). 


[  Cocci.     ] 

■j  Bacilli.   1-  Bacteria. 

[  Spirilla.  J 


Animal 
kingdom 


Lowest  forms 


Protozoa:  single  cells 
without  circulatory  or 
nervous  systems. 


f  Sarcodinea. 
!  Flagellata. 
I  Sporozoa. 
I  Infusoria. 


Mycetozoa,  fungi  not  certainly  defined  as  animal  or  vegetable  forms.' 


Higher  forms.     Certain  insect  and  worm  forms  are  pathogenic. 


Of  the  protozoa  four  classes  are  known, 
though  but  few  species  are  pathogenic;  these 
classes  are  (1)  the  sarcodinea  (ameboid), 
which  includes  the  ameba  coli  of  dysentery 
(Fig.  10);  (2)  the  flagellata,  non-ameboiti 
but  motile  by  means  of  flagella;  (3)  the 
sporozoa  living  within  the  bodies  of  other 
animals,  a  class  which  includes  the  hemo- 
sporidia,  ameboid  motile  parasites  living  in 
the  blood,  and  of  which  the  malarial  germs, 
Plasmodium  malaria  (quartan  fever,  seventy- 
two-hour    cycle),   the    plasmodium    precox 


Fig.  6 


Trichophyton  tonsurans, 
("barber's  itch").  Diagram- 
matic.    (Lehmann.) 


>  The  terms  mycetozoa  and  protozoa  seem  to  be  practically  synonymous  to  pathologists,  who 
use  the  term  protozoa  in  the  sense  of  mycetozoa  as  above  defined. 


36       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 


(estivo-aiitumnal  fever,  twenty-four  or  forty-eight-hour  cycle,  Fig.  11), 
the  cytorcytes  variolae  seu  vaccinae  (the  probable  cause  for  smallpox 
and  chickenpox)  are  examples;  (4)  the  infusoria. 


Fig.  7 


Fig.  8 


Penicillium  with  spores.    (Lehmann.) 
Fig.  9 


a,  saccharomyces;  b,  cell  with  four 
spores.    (Lehmann.) 

Fig.  10 


Saccharonnyoes  albicans.     (After  Grawifcz,  in  Leliinann.) 


1,  ameba  from  dysenteric 
stool,  with  vacuoles  and  enclosed 
red  cells;  2,  ameba  from  straw 
infusion;  3,  the  same  encysted 
X  600.     (Kiinster.) 


The  vegetable  fungi  are  divided  into  (1)  schizomycetes,  or  fission 
fungi;  (2)  hyphomycetes,  or  mould  fungi  (Figs.  6  and  7);  (3)  blasto- 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE      37 

mycetes,  or  bud  fungi  (or  yeasts)  (Figs.  8  and  9).  Being  without 
chlorophyll,  the  fungi  are  unable  to  utilize  the  simple  compounds, 
•  such  as  carbon  dioxitle  and  ammonia,  as  foods,  and  are  therefore 

Fig.  11 


Plasmodium  precox  (forty-eight  hours). 
Cycles  of  estivo-autumtuil  parasite.  1.  Very  young  form.  2.  Infection  of  one  cell  with  seven 
young  parasites.  (Drawn  from  a  marrow  smear.)  3.  Triple  infection;  two  parasites  joined 
by  single  chromatin  mass.  4.  Double  infection;  peculiar  rings  with  two  chromatin  grains  at 
opposite  poles.  5.  Double  infection;  small  ring  adherent  to  cell.  6,  7.  Signet-ring  forms; 
subdivision  of  chromatin.  8,  9.  Later  ring  forms,  with  subdivided  chromatin  and  few  pigment 
grains.  10-12.  Full-grown  forms  with  finely  subdivided  chromatin  and  gradual  concentration 
of  pigment.  13,  14.  Stages  of  presegmenting  forms,  with  concentrated  eccentric  pigment.  15. 
Double  infection  with  separate  presegmenting  bodies.  16.  Estivo-autumnal  rosette.  17,  18. 
Young  crescent  and  ovoid.  19.  "Pulsating"  crescent.  20-22.  Various  forms  of  crescents.  23. 
Two  bows  about  single  crescent.  24.  Fully  developed  crescent;  two  masses  of  chromatin; 
achromatic  substance;  double  wreaths  of  pigment.  25.  Diagrammatic  flagellating  body. 
26.  Extracellular  sterile  body.     (Schmaus  and  Ewing.) 

compelled  to  break  down  the  complex  organic  compounds,  for  which 
purpose  they  are  competent.  All  three  classes  of  fungi  have  repre- 
sentatives which    produce    disease    m    the  human    body,   but    the 


38      MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 
schizomycetes  furnish  by  far  the  greater  number  of  infectious  disease 


causes. 


^  Chemically,  bacteria  are  about  85  per  cent,  water,  together  with 
albumin  called  mycoprotein,  ferments,  soluble  extractives,  salts, 
sometimes  nuclein  basis,  coloring  matters,  organic  acids,  sulphur 
starch,  and  cellulose. 


Fig.  12 


o,  spiral  forms  with  a  flagellum  at  only  one  end;  b,  bacillus  of  typhoid  fever  with  flagella  given 
off  from  all  sides;  c,  large  spirals  from  stagnant  water  with  wisps  of  flagella  at  their  ends 
(spirillum  undula).     (Abbott.) 

The  schizomycetes  (Greek  schizo,  to  split,  and  mukes,  a  fungus) 
are  minute  single-celled  plants  without  nuclei,  but  possessed  of  a  cell 
wall  and  cell  protoplasm  (mycoprotein).  They  have  a  size  of  about 
1  micron  (1/^  =  ■25"¥To'  '^^^)  *^^  ^^^^  ^^  ^^^^^  smallest  diameter. 
Some  of  them  possess  flagella,  hair-like  processes,  often  very  numerous. 

Fig.  13 


Typhoid  bacilli — stained  by  Van  Ermengem's  method  to  show  flagella. 

arising  from  the  protoplasm  rather  than  the  wall,  with  which  they  lash 
the  fluid  surrounding  them,  and  by  which  means  they  effect  locomotion 
(Fig.  12).  Other  bacteria  again  are  non-motile.  Entering  the  organic 
compounds,  carbohydrates,  hydrocarbons,  and  nitrogenous  (albu- 
minous) substances,  they  ferment  or  decompose  them,  forming  new 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE      39 

products,  and  extract  from  tliem  substances  necessary  to  their  growth 
and  subseciuent  reproduction.  The  substance  in  which  they  thus  grow 
is  called  the  medium  or  soil.  The  conditions  under  which  this  is  accom- 
plished are :  (1 )  The  fungi  must  have  a  proper  vitality.  (2)  Their  food 
supply  or  soil  must  be  suited  to  their  growth  and  must  be  moist — in 
general  terms  they  require  water,  C.N.O,  and  salts.     (3)  The  tempera- 

FiG.  14 


0000  qO 


o°0  "oS    <^o 

*  .8  .  *f 

'9^„(s>     eF>       (f> 

<y>     ^0   °°° 

Op 

gg     00 

c  d  e 

a,  stapJiylococci;  b,  streptopocci;  c,  diplococci;  rf,  tetrads;   e,  sarcina".     (Abbott.) 

ture  must  be  suitable;  they  grow  more  actively  at  about  102°  F. ;  at 
160°  F.  maintained  they  usually  die,  but  in  some  cases,  as  with  the 
typhoid  bacilli,  they  may  live  in  the  spore  form  at  even  212°  F.  or  over 
unless  maintained  for  some  time.  Some  that  develop  best  at  high  tem- 
perature are  called  thermophilic.  Low  temperature,  as  32°  F.  or  far 
below,  that  inhibits  their  growth,  but  does  not  necessarily  kill  them. 
(4)  Their  waste  products  must  be  removed  or  they  die  in  them.  This 
is  said  to  be  due  to  the  reaction,  whether  acid  or  alkaline,  and  not  to 
any  of  the  other  by-products — e.  g.,  in  lactic  fermentation  2  per  cent, 
of  lactic  acid  is  about  the  greatest  amount  endured  by  them.     They 

Fig.  15 


if-r—  ~.>;1  V/  --'r- >v-  / 

ZooKlea  of  bacilli.      (Abbott.) 

are  also  sensitive  to  and  inhibited  by  agitation,  daylight,  electric 
light,  and  electrical  currents.  ^Morphologically  the  schizomycetes  are 
grouped  into  several  classes  according  to  form. 

1.  Micrococci  (mikros,  and  kokkos,  a  berry),  including  all  of  the 
spherical  forms  or  those  having  equal  or  nearly  equal  diameters 
(Fig.  14). 


40       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

2.  The  bacilli  (bacillum,  a  rod),  or  rod-like  forms;  one  diameter 
being  greater  than  the  other  (Fig.  16). 

3.  The  spirilla  (Greek  spira,  a  coil),  or  the  curved  forms  (Fig.  17). 
All  of  these  groups  may  again  be  subdivided.    The  micrococci  are 

subdivided  according  to  their  modes  of  grouping.  Double  cocci  are 
called  diplococci  (diploos,  double).  If  in  division  the  cocci  agglom- 
erate like  a  bunch  of  "grapes,  they  are  called  staphylococci  {staphyle, 


'9  .-^y.-.-- 


Fig.  16 


I'J      '<h     >v»      -;V 


o  b  c  d 

a,  bacillus  subtilis  with  spores;  6,  bacillus  anthracis  with  spores;  c,  Clostridium  with 

spores;   d,  bacillus  of  tetanus  with  spores. 

a  grape).  If  they  arrange  themselves  in  a  chain,  they  are  called  strep- 
tococci {streptos,  a  chain).  If  they  divide  in  two  directions  and  form 
a  bunch  of  four  cocci,  they  are  called  tetrads.  If  in  three  directions, 
they  form  sarcinse.  The  bacilli  are  of  many  and  varied  forms,  and 
differ  as  to  their  mode  of  grouping.  During  reproduction  bacteria 
may  excrete  a  material  which  unites  them  into  a  gelatinous  mass 
called  zooglea. 

The  bacilli  in  the  course  of  reproduction  may  form  long  threads 
showing,  as  a  rule,  the  traces  of  segmentation.  Under  certain  unfa- 
vorable conditions  the  development  of  many  bacilli  form  glistening 
oval  bodies  within  themselves  (endospores)  which  resist  stains.     The 

Fig.  17 

a  b 

a,  spirillum  of  Asiatic  cholera  (comma  bacillus);  h,  involution  forms  of  this  organism 
as  seen  in  old  cultures.     (Abbott.) 

body  of  the  bacillus  may  disappear,  leaving  the  spore  only.  These 
spores  are  very  resistant  to  devitalizing  agents.  The  bacilli  forming 
spores  are  said  to  be  in  the  resting  stage.  These  spores  under  favor- 
able conditions  again  form  bacilli  like  their  progenitors,  but  do  not 
form  other  spores  without  this  return  to  the  bacillus  form.  A  single 
cell  forms,  as  a  rule,  but  one  spore.  Some  bacilli  do  not  form  spores 
(Abbott). 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE       41 

If  the  entire  bacterium  is  changed  into  the  spore  form  they  are  called 
arthrospores,  when  cocci  take  on  the  appearance  of  spores  they  are 
also  called  arthrospores.  Under  unfavorable  conditions  bacteria  may 
undergo  degeneration  and  take  on  abnormal  or  involution  forms,  and 
when  the  conditions  are  again  favorable  to  development  they  may 
resume  their  typical  forms/  While  these  form  changes  occur,  bac- 
teria are  never  permanently  changed  from  one  form  to  another.^ 
Those  bacteria  which  have  several  forms  in  their  life  cycle  are  termed 
pleomorphic.  Those  having  but  one  form  are  monomorphic.  Those 
bacteria  which  exist  on  living  tissue  are  known  as  parasitic.  They 
enter  the  body  by  way  of  open  wounds  or  surfaces  deprived  of  epithe- 
lium, or  may  lodge  at  certain  points  of  the  mucous  surface  of  the 
lungs,  skin  openings,  or  the  alimentary  canal.  If  not  killed  out  they 
multiply  in  the  natural  juices  of  the  part  on  which  they  locate  and 
produce  an  infective  inflammation.  Poisonous  substances  may  be 
generated,  which  are  absorbed  into  the  system  and  may  act  as  poisons, 
producing  toxemia.  When  the  toxin  is  excreted  by  the  bacteria  and 
floats  in  the  blood  it  is  called  extracellular  toxin ;  when  confined  to  the 
bacteria,  it  is  called  endotoxin. 

The  character  of  both  the  inflammation  and  the  poisoning  depends 
upon  the  particular  bacterium  or  bacteria  present.  The  bacteria  may 
in  certain  cases  be  taken  into  the  blood,  and,  coming  to  rest  at  certain 
spots,  the  above-described  process  is  repeated. 

The  Bacillus  anthracis  divides  in  the  blood  stream,^  and  other 
organisms,  such  as  the  Bacterium  pneumoniae  and  Bacillus  influenzae 
may  exist  in  it.  Many  forms  of  organisms  exhibit  a  preference  for 
certain  spots  at  which  they  find  the  conditions  best  suited  to  develop- 
ment— e.  g.,  the  typhoid  bacillus  in  the  glands  of  the  ileum,  Beyer's 
patches;  the  anthrax  bacillus  in  the  lungs  of  animals;  the  diphtheria 
bacillus  in  the  mucous  surfaces  of  the  pharynx  and  contiguous  parts. 
Those  parasitic  bacteria  which  produce  disease  are  called  pathogenic, 
others  are  non-pathogenic. 

The  mouth  offers  a  suitable  habitat  for  many  bacteria. 

The  bacteria  which  live  on  dead  organic  matter  are  called  sapro- 
phytic {sapros,  rotten,  antl  phidon,  a  plant).  They  break  up  the  dead 
animal  and  vegetable  matter  into  simple  compounds  like  carbon 
dioxide,  ammonia,  etc.,  which  are  utilized  by  the  higher  chlorophyl- 
lous  plants.     The  nitrogen  of  the  air  is  also  utilized  by  some  plant 

1  Abbott.  *  Abbott. 

*  Green,  Pathology  and  Morbid  Anatomy. 


42       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

bacteria,  and  can  be  introduced  to  aid  crops.  As  animals  are  depend- 
ent upon  plants  for  existence,  their  vast  importance  in  the  economy 
of  nature  is  evident.  Bacteria  may  often  pass  from  a  parasitic 
existence  to  a  saprophytic  one — a  fact  which  is  utilized  in  their  study 
by  bacteriologists,  who  prepare  artificial  media  in  which  to  cultivate 
them.  These  are  called  cultures,  which  by  transference  from  one 
culture  plate  to  another  of  like  kind  are  said  to  be  passed  through 
generations.  When  by  careful  segregation  one  form  of  bacterium  is 
separated  from  others  present  in  a  mixed  culture  and  thereafter  cul- 
tivated alone,  it  is  called  a  pure  culture;  when  the  bacteria  are  thinly 
spread  on  a  gelatin  or  agar  culture  and  then  isolated,  the  grouped 
bacteria  developing  at  each  point  are  called  a  colony.  Bacteria  may 
pass  from  a  saprophytic  to  the  parasitic  form  of  existence.  Bacteria 
which  have  this  power  of  adaptation  to  a  new  form  of  medium  are 
called  facultative.  When  without  this  power,  they  are  obligate  bacteria. 

According  to  Pasteur,  those  which  require  oxygen  in  order  to  live 
are  called  aerobic.  Those  which  cannot  live  in  its  presence  are  an- 
aerobic.   Those  which  live  either  way  are  facultative. 

When  bacteria  produce  pigment  either  within  themselves  or  their 
medium,  they  are  termed  chromogenic;  when  they  produce  light  or 
phosphorescence,  they  are  termed  photogenic.  If  they  have  the  ability 
to  produce  fermentation,  they  are  termed  zymogenic;  when  they 
produce  gas,  they  are  called  aerogenic. 


FERMENTATION. 

Fermentation  in  the  broadest  acceptation  of  the  term  has  been 
defined  as  the  decomposition  of  substances  possessing  complex  mole- 
cules under  the  influence  of  organized  or  unorganized  ferments 
(enzymes).  The  decompositions  occur  when  organic  substances  are 
exposed  to  the  action  of  bacteria  or  their  enzymes,  or  are  subjected  to 
the  action  of  certain  ferments  such  as  are  found  in  the  digestive  fluids 
secreted  into  the  alimentary  canal,  which  are  really  enzymes  also 
derived  from  living  cells. 

According  to  Woodhead,*  the  molecules  of  the  fermented  compovmd 
are  separated  from  one  another  for  a  brief  period  and  then  allowed  to 
combine  and  form  simpler  and  more  stable  compounds.  The  process 
is  accompanied  by  heat  due  to  chemical  changes. 

I  Bacteria  and  their  Products. 


FERMENT  A  TIOX  43 

Ferments,  then,  are  of  two  kinds:  (1)  organized  or  formed  ferments 
or  living  bacteria  which  muhiply  at  the  expense  of  the  substance 
which  they  are  fermenting;  (2)  unorganized  or  unformed  ferments 
or  enzymes,  nitrogenous  bodies  produced  by  Hving  cells  which  have 
the  power  of  producing  chemical  changes  in  organic  substances.  They 
thus  affect  many  times  their  own  weight  of  the  particular  organic 
substance  being  fermented  without  being  themselves  much  affected, 
though  eventually  exhausted.  Typical  examples  are  the  pepsin  of 
the  gastric  juice,  which  changes  albumin  to  peptone,  and  the  ferment 
of  the  yeast  plant,  proved  capable  of  changing  sugar  into  alcohol  and 
carbon  dioxide,  even  when  the  cells  themselves  are  crushed  and 
filtered  out. 

The  unorganized  ferments  usually  act  by  oxidizing,  deoxidizing, 
or  hydrating  the  substance  modified.  They  act  best  when  their 
products  are  removed  from  their  neighborhood. 

Many  bacteria  have  been  shown  to  possess  such  unorganized  fer- 
ments. It  is  probable  that  they  produce  their  effects  on  organic  sub- 
stances by  the  aid  of  these  ferments,  which  serve  them  as  pepsin  serves 
man  (extra  cellular  ferments).  It  is  thought  that  in  other  cases  the 
germs  take  up  organic  food,  digest  it,  and  excrete  waste  products 
in  somewhat  the  same  manner  that  the  body  cells  nourish  them- 
selves by  intracellular  ferments.  As  a  rule,  more  than  one  species 
of  bacterium  infects  a  fermentable  substance.  The  more  active 
varieties  predominate  in  the  fermentation,  but  mixed  fermentations 
may  proceed.  In  some  cases  the  bacterial  multiplication  is  favored  by 
the  activity  of  other  bacteria,  in  some  cases  the  development  is  retarded. 
Some  may  die  out,  finding  an  unfavorable  soil.  After  a  time  the  pre- 
dominating bacteria  may  die  in  the  waste  products  accumulated  about 
them,  leaving  the  field  clear  for  a  second  or  third  variety.  In  this  way 
progressive  decompositions  may  occur — c.  g.,  the  alcoholic  fermenta- 
tion may  be  succeeded  by  the  acetic,  in  which  the  alcohol  is  changed 
to  acetic  acid,  as  in  cider- vinegar  formation.  The  nature  of  the  chem- 
ical changes  produced  in  a  fermentable  substance  depends  upon  the 
chemical  nature  of  the  latter  and  upon  the  nature  of  the  fungus  causing 
the  fermentation. 

Thus,  in  an  infusion  of  vegetable  juices  containing  sugar  a  yeast 
fungus  (one  of  the  blastomycetes)  will  produce  carbon  dioxide  gas  and 
alcohol  if  the  oxygen  of  the  air  be  freely  admitted  (aerobiosis),  while 
if  to  a  fresh  portion  of  the  same  solution  scrapings  from  carious 
dentine  be  added,  lactic  acid  will  be  formed  and,  as  a  rule,  no  gas. 


44      MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

Moreover,  the  reaction  will  occur  if  oxygen  be  excluded  (anaerobiosis). 
In  albuminous  compounds  an  alkaline  reaction  and  entirely  different 
substances  will  be  formed  upon  the  addition  of  carious  dentine. 

The  ferments  produced  by  bacteria  are  quite  numerous. 

The  'proteolytic  ferment  dissolves  albuminous  substances;  proceeds 
under  an  alkaline  reaction  and  sometimes  under  an  acid  reaction. 

The  diastatic  ferments  change  starch  into  sugar. 

diverting  enzymes  convert  saccharose  into  dextrose  or  non-ferment- 
able forms  of  sugar  to  fermentable  ones. 

Coagulating  ferments  coagulate  milk.  Coagulation  is  also  produced 
in  the  tissues  and  exudate  in  inflammation  by  the  ferments  of  pyogenic 
cocci. 

Sugar-splitting  ferments  change  sugar  into  other  products,  as 
alcohol,  carbon  dioxide,  and  lactic  acid. 

Fat-splitting  ferments  split  fats  into  glycerin  and  fatty  acids. 

Hydrolytic  ferments  cause  a  combination  with  the  elements  of  water 
in  substances  they  decompose. 

Emidsifying,  oxidizing,  and  nitrifying  ferments  also  occur. 

Toxins  are  also  classed  with  the  ferments,  and  are  capable  of 
producing  new  substances  when  distributed  in  the  blood.  (See 
Immunity.) 

The  progressive  decomposition  of  albuminous  matter  into  simple 
compounds  is  effected  by  many  bacteria  through  processes  of  oxida- 
tion, deoxidation,  and  hydration. 

Peptones^  are  first  formed,  next  alkaloid-like  bodies  called  pto- 
maines; succeeding  this  such  nitrogenous  bases  as  leucin,  tyrosin,  and 
the  amines  (methyl,  ethyl,  and  propylamine)  are  formed;  next  fatty 
acids  and  such  acids  as  butyric,  lactic,  and  succinic  acid  appear; 
next  aromatic  products  such  as  indol,  phenol,  and  cresol  are  formed, 
and  the  final  decomposition  is  represented  in  the  end  products — carbon 
dioxide,  CO2;  hydrogen  sulphide,  HjS;  ammonia,  NH3;  and  water, 
H2O.  When  bacteria  produce  decomposition  of  living  animal  tissue, 
they  effect  this  putrefaction,  as  distinctly  noted  in  certain  cases  of 
abscess. 

Such  products  of  bacterial  action,  either  produced  in  a  living  or  a 
saprophytic  medium,  as  are  capable  of  acting  as  poisons  in  the  animal 
organism  are  called  toxins.  Some  animal  parasites  also  produce  them. 
It  is  understood  that  they  differ  according  to  the  fungus  and  the 
medium.    If  the  toxin  be  proteid  in  nature,  it  is  termed  a  toxalbumin. 

i  Ziegler'a  General  Pathology. 


MICROCYTES 


45 


Some  of  the  ptomaines  are  toxic;  the  greater  number  are  not. 

When  the  toxins  alone  are  absorbed  from  a  focus  of  infection  the 
subject  is  poisoned — a  condition  called  toxemia,  whether  due  to' a 
toxic  ptomaine,  as  in  the  case  of  Asiatic  cholera,  or  to  a  toxalbumin, 
as  in  the  case  of  diphtheria.  Such  toxemia  is  commonly  accompanied 
by  more  or  less  fever,  according  to  the  amount  taken  up.  ^Mien  the 
organisms  enter  the  circulation  and  multiply  in  the  blood,  or  at  least 
move  about  and  live  in  it,  to  be  carried  to  capillaries  in  which  they  can 
rest  and  multiply,  the  condition  is  termed  a  septicemia.^  In  toxemia 
and  septicemia  the  symptoms  depend  upon  the  nature  of  the  organism 
and  their  products.  Bacteria  are  found  everywhere  and  exist  upon 
the  surface  of  the  body,  in  its  external  cavities,  and  in  the  alimentary 
canal.    Here  under  conditions  of  health  there  seem  to  be  conditions 

Fig.   18  Fig.   19 


Staphylococcus    pyogenes   aureus.        From    a 
culture.      X  1000.     (Green.) 


Streptococcus  pyogenes.      From   pus  found 
in  a  pyemic  abscess.    X  1000.     (Green.) 


favoring  certain  forms,  which,  wlien  implanted,  occupy  the  field  and 
exclude,  except  temporarily,  other  forms  to  which  the  soil  is  not  so 
well  suited.  These  are  known  as  the  "normal  flora."  It  has  been 
shown,  however,  that  the  growth  of  some  bacteria  is  favored  by  the 
presence  of  certain  otliers  (symbiosis). 

With  certain  changes  occurring,  other  forms  may  become  implanted. 
Pathogenic  bacteria  may  exist  in  the  healthy  cavities  and  produce  no 
ill  results.  Again,  the  soil  mav  favor  and  disease  l)eo;ins.  Certain  bac- 
teria  have  been  found  constantly  present  in  relation  with  certain  dis- 
eases— e.  g.,  the  spirillum  of  Asiatic  cholera  with  that  disease.  These 
are  specific  bacteria.  Taken  from  individuals  with  the  disease,  they 
produce  it  in  susceptible  animals  inoculated  with  them  if  circumstances 
favor  their  growth. 

»  Abbott. 


46       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 


Bacteria  spread  in  the  tissue  along  the  Hnes  of  least  resistance. 
They  may  follow  the  cellular  tissue  or  enter  the  lymphatics,  or  pass 
at  once  into  the  veins  and  be  carried  into  the  circulation.  They  may 
be  strictly  localized  at  the  point  of  infection. 

Thus  there  may  be  a  localized  inflammation— e.  g.,  in  simple  abscess 
due  to  the  Staphylococcus  pyogenes  aureus;  a  diffuse  inflammation, 
as  in  case  of  infection  by  the  Streptococcus  pyogenes;  a  gland  infection 
or  septicemia,  as  in  anthrax  or  general  infection  by  Streptococcus 
pyogenes  or  Bacterium  pneumoniae;  or  a  metastatic  inflammation,  as 
in  pyemia,  in  which  the  germs  (usually  Streptococcus  pyogenes)  gain 
access  to  the  blood  from  a  local  focus  of  infection  and  are  carried  to 
distant  parts,  in  which  they  cause  abscesses  while  the  products  pro- 


FiG.  20 


fern 

Mouse's  lung;  vessels  plugged  with  bacilli  anthracis:     a,  alveolus;  v,  vein  full  of  bacilli; 
c,  capillaries  also  full;  hr,  bronchus.      X  400.    (Horsley.) 

duce  toxemia.  To  produce  effect,  germs  in  the  blood  must  come  to 
rest  at  some  point,  which  may  occur  in  the  capillaries  owing  to  their 
injury,  in  thrombi  or  emboli,  or,  in  case  of  entrance  of  bacteria  into  a 
leukocyte,  they  may  migrate  into  the  connective  tissue  (Fig.  20). 

It  has  been  shown  that  pyogenic  germs  may  exist  in  the  blood  with- 
out local  effects,  while  again  a  local  injury  may  cause  the  arrest  of  the 
germs  and  a  secondary  local  inflammation  or  abscess  be  set  up.  This 
is  due  to  simple  arrest  or  to  extravasation  of  blood,  which  permits  the 
germs  to  pass  from  the  vessels  into  the  connective  tissue. 

General  or  local  depression  of  tissue  vitality  acts  as  a  predisponent 
to  local  infection. 

The  infections  themselves  are  classified  as  primary,  secondary,  and 
mixed. 


BACTERIA  OF  THE  MOUTH  47 

The  primary  is  the  original  infection,  say,  e.  g.,  Bacilkis  tubercu- 
losis. The  secondary  is  that  implanted  when  the  original  disease  is 
well  under  way — e.  g.,  Streptococcus  pyogenes  aureus  upon  tul)er- 
culosis;  a  third  or  tertiary  infection  is  possible/ 

The  original  infection  may  be  by  mixed  germs,  more  than  one  of 
which  may  multiply.  Thus,  the  Streptococcus  pyogenes  aureus  and 
Bacterium  pneumonia^  may  both  be  found  in  an  abscess.  This  is  a 
mixed  infection. 

BACTERIA  OF  THE  MOUTH. 

In  even  the  best  cared  for  mouths  bacteria  are  numerous  and  find 
the  conditions  suited  to  their  growth.  In  unclean  mouths  containing 
food  debris,  dead  epithelium,  etc.,  their  life  conditions  are  much  more 
favorable. 

According  to  Miller^  there  are  a  number  of  bacteria  which  almost 
invariably  occur  in  every  mouth.    These  are: 

1.  Leptothrix  innominata. 

2.  Bacillus  buccalis  maximus. 

3.  I^eptotlirix  buccalis  maxima. 

4.  Jodococcus  vaginatus. 

5.  Spirillum  sputigenum. 

6.  Spirochete  dentium  (denticola). 
To  this  list  Goadby^  has  added: 

I^eptothrix  racemosa  of  Vicentini,  further  described  by  Williams.* 

Streptococcus  brevis  of  Lingelsheim  and  Cladothrix  buccalis  (pro- 
visionally added). 

With  the  exception  of  Streptococcus  brevis  and  perhaps  Cladothrix 
and  Bacilli  buccalis  maximus,  these  are  uncultivable  on  laboratory 
media,  are  strictly  obligate  parasites.  Of  the  last-named  organism 
Goadby  obtained  biological  characteristics  of  the  pure  culture,  but  (Hd 
not  establish  its  disease-producing  power,  if  any. 

Certain  pathogenic  organisms  have  been  shown  to  be  present  in 
the  mouths  of  healthy  persons,  such  as  bacteriological  investigators; 
tliose  nursing  infectious  diseases,  such  as  diphtheria,  scarlet  fever,  etc., 
and  even  in  the  mouths  of  healthy  individuals  apparently  not  exposed 
to  any  infection.  In  about  10  per  cent,  of  all  individuals  examined  at 
random  Netter  found  Sta])hylococcus  pyogenes  aureus  (golden  pus). 
Staphylococcus  pyogenes  albus  was  also  found.     The  Pneumococcus, 

>  Park,  Surgery  by  American  Authors.  -  Microorganisms  of  the  Human  Mouth. 

3  Mycology  of  the  Mouth,  1903.  *  Dental  Cosmos,  1899.    See  Dental  Caries. 


48       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 


Fig.  21 


or  Bacterium  pneumonise,  was  found  in  the  mouths  of  about  15  per  cent, 
of  healthy  individuals.  This  organism  has  been  found  by  Kirk  to 
be  apparently  causative  of  pericemental  abscess,  and  has  been  reported 
by  Schreier^  as  found  in  75  per  cent,  of  cases  of  apical  abscess  exam- 
ined. It  has  also  been  related  with  cases  of  osteomyelitis.  The  Bacillus 
diphtherise  of  Loeffler  has  been  found  in  about  10  per  cent,  of  mouths 
examined  at  random,  and  33  per  cent,  of  600  children  in  a  school 

examined  during  an  epidemic  of  diph- 
theria were  found  to  have  the  bacillus 
present  in  the  mouth,  while  but  about 
2  per  cent,  developed  the  disease.^ 
This  latter  fact  shows  the  absolute 
necessity  for  a  predisposition  as  well 
as  an  exciting  cause. 

The  Bacillus  tuberculosis  exists  in 
the  mouths  of  many  suffering  from 
pulmonary  tuberculosis ,  and  exists  also 
at  times  in  the  mouths  of  the  healthy. 
Primary  tuberculous  osteitis  has  been 
The  SaccharOmyces  albi- 

a  section  of  lung  in  the  "red  hepatization"  ^^^^  ^^    prCSCUt    and    at     timCS 

stage  of  acute  pneumonia.      In  the  upper  ''  '■ 

part  of  the  field  is  a  cell  containing  several  produCC  thrUsh   (Fig.   9). 

cocci — possibly   a   phagocyte.        X  1000.  mi       n       -n        j.       i  /j.       i      •  i\  i 

(Qreen.)  ^  ^^  Bacillus  typhosus  (typhoid)  has 

been  found  in  the  healthy  mouth,  and 
at  times  has  oral  pathogenicity.  Many  other  organisms  have  been 
isolated  from  the  human  mouth.  Some  of  these  have  specific  char- 
acter, of  others  little  is  known.  Some  of  the  bacteria  of  the  mouth 
possess  the  power,  under  certain  conditions,  of  felting  themselves 
in  gelatinoid  masses  or  films  upon  the  surfaces  of  the  teeth.  Here, 
if  properly  supplied  with  carbohydrate  food,  some  of  them  produce 
lactic  acid  and  decalcify  the  teeth.  Some  of  the  masses  may  de- 
velop an  alkaline  reaction  due  to  putrefaction.  Some  have  a  later 
putrefactive  action  upon  the  organic  matrix  of  the  dentine.  Goadby^ 
gives  an  interesting  classification  of  bacteria  found  in  dental  caries 
(which  see).  Some  bacteria  not  yet  isolated  are  the  probable  causes 
of  pyorrhea  alveolaris. 

The  bacteria  in  the  mouth  probably  are  taken  into  the  food  and 
swallowed  in  great  numbers.    Many  are  doubtless  killed  by  the  gas- 


Diplococci  pneumoniEB  entangled  in  the       ,  , 

mashes  of  the  fibrinous  exudation.     From     ODServeu. 


'  Dental  Co.'smos,  1893. 
'  Mycology  of  the  Mouth, 


2  Cioadby. 


BACTERIA  OF  THE  MOUTH 


49 


trie  juice,  which  is  a  weak  germicide;  notwithstanding,  some  pyogenic 
cocci  and  some  of  the  blastomycetes  may  develop  in  the  stomach  and 
produce  disease.     Many  also  may  enter  the  intestines  and   either 


Fig.  22 


Bacillus  (liphtherise:   A,  its  morphology  on  glycerin-agar-agar;    B,  its  morphology  on  Loeflaer'; 
blood  serum;    C,  its  morphology  on  acid  blood-serum  mixture.    (Abbott.) 


Fig.  23 


\ 

/ 


/ 


> 


excite  disease  of  specific  character  or  produce  abnormal  intestinal 
fermentations,  the  toxins  of  which  may  be  absorbed,  and  produce 
malnutritional  conditions.  They  may  remain  localized  in  the  mouth 
and  produce  oral  disease,  dental  caries,  or  peri- 
cemental diseases,  etc.  Collections  upon  the 
teeth,  plates,  etc.,  abscesses,  pyorrheas,  etc.,  are 
unquestionably  the  causes  in  many  instance.s 
of  fever,  septic  infection,  intestinal  disturb- 
ances, heart  complications,  pulmonary  tuber- 
culosis, glandular  enlargements,  etc.  The 
relation  of  an  unclean  mouth  to  effects  upon 
the  mouth  and  alimentary  canal  and  air  pas- 
sages is,  therefore,  a  direct  one  of  an  import- 
ance that  renders  exact  studios  in  this  direction 
of  extreme  value.  The  saliva,  while  not  germicidal  (^Miller),  may  or 
may  not  contain  substances  acting  as  pabulum  for  the  growth  of 
bacteria,  but  probably  does  in  many  cases  apart  from  extraneous 
food  materials  introduced. 
4 


Bacillus  tuberculosis. 
X  1000.      (Green.) 


50       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

THE  RESISTANCE  OF  THE  TISSUES  TO  INFECTION. 

The  resistance  of  the  tissues  to  bacteria  is  to  be  considered  from 
two  main  standpoints :  (1)  The  prevention  of  the  entrance  of  bacteria 
into  the  tissues.  (2)  The  destruction  of  the  bacteria  after  entrance 
into  the  tissues. 

1.  The  prevention  of  entrance.  It  has  been  shown  that  pathogenic 
bacteria  may  enter  the  mouth,  alimentary  canal,  lungs,  etc.,  but  few 
develop. 

The  skin  acts  as  a  mechanical  barrier,  though  its  opening  may  at 
times  harbor  bacteria. 

The  mucous  membrane  secretes  mucus,  which  envelops  bacteria 
and  with  it  they  are  carried  away.     The  healthy  mucus  also  has 

Fig.  24 


1,  a  spore  which  has  penetrated  the  intestinal  wall  and  entered  the  abdominal  cavity,  where 
four  leukocytes  have  surrounded  its  end:  m,  the  muscular  layer  of  the  intestine;  e,  epithelial 
layer;  s,  the  serous  layer;  2,  a  spore  surrounded  by  leukocytes  from  the  abdominal  cavity  of 
a  Daphne.     (Metchnikoff.)  ^ 

apparently  a  devitalizing  power  for  some  bacteria,  not  for  others. 
The  acid  gastric  juice  kills  many,  but  some  may  pass  through  two  or 
three  hours  after  a  meal,  at  times  when  the  gastric  juice  is  not  active. 
Probably  the  intestinal  juices  also  inhibit,  in  large  degree,  the  action  of 
such  as  have  entered  the  alimentary  canal.  In  all  cases  the  agitation 
of  the  fluids  of  a  part  seems  to  act  mechanically  to  prevent  localization 
of  bacteria. 

2.  The  prevention  of  development  in  tlie  tissues.  Within  the 
healthy  tissues  bacteria  find  several  elements  opposing  their  develop- 
ment. 

It  seems  the  consensus  of  opinion  of  pathologists  that  the  blood 
serum  normally  contains  germicidal  substances  probably  of  the 
nature  of  a  nuclein  and  called  by  Buchner  "alexins." 

This  belief  is  mainly  based  upon  the  demonstration  of  Nuttall  that 
filtered  blood  serum  possesses  the  power  of  producing  the  degenera- 
tion of  l^acteria.  Bnchnor  found  that  heating  to  55°  C.  destroyed 
this  property,  a  fact  pointing  to  the  albuminous  nature  of  the  alexins. 


THE  RESISTANCE  OF   THE   TISSUES   TO  IXFECTIOX 


51 


Fig.  25 


After  reviewing  all  the  evidence,  Vaughan  and  Xovy'  conclude:  "(1) 
the  exact  nature  of  the  germicidal  constituents  of  the  blood  or  alexins 
is  not  known;  (2)  the  alexins  have  their  origin  in  the  white  blood  cor- 
puscles; (3)  disintegration  of  the  white  l)lood  corpuscles  liberates 
alexins;  (4)  it  is  probably  true  that  alexins  are  also  secreted  by  living 
leukocytes." 

Metchnikoff,  in  1SS4,  demon- 
strated that  the  leukocytes  take 
up  bacteria  within  themselves  and 
claimed  that  they  thus  destroy 
them.  This  process  he  termed 
phagocytosis  {phago,  I  eat;  ci/tos, 
a  bud).  It  is  now  considered  that 
this  property,  which  is  also  pos- 
sessed by  the  endothelial  cells  of 
the  bloodvessels  and  by  the  fibro- 
blasts, is  but  evidence  of  the  nu- 
tritive function  of  simple  cells 
occurring  after  the  bacteria  have 
been  partially  degenerated  by  the 
serum  (Fig.  25).  This  is  borne 
out  by  experiments:  ]\Iixed  pyo- 
genic cocci    and  leukocvtes   free 

°  .'  .   .  Active  phagocytosis.      Endothelial  cells  en- 

from     blood    serum    exhibiting    no    dosing  the   bacilli   of  swine   septicemia,   from 

nhno-nrvfir  qetlvitv  wherens  when  i"  hepatic  vein  of  a  pigeon:  a,  endothelial 
pnagoc}  tic  acti\  U} ,  w  neieas  w  nen  ^^j,^.  ^  ip^j^^cytes.   (Metchnikoff.) 

the  bacteria  are  first  exposed  to 

blood  serum  and  then  to  phagocytes,  there  is  marked  phagocytosis.' 

Researches  of  Leber,  Buchner,  and  others  have  shown  that  leuko- 
cytes may  be  attracted  by  certain  bacterial  products  even  in  high  iHlu- 
tion,  and  by  other  chemical  substances  such  as  mercury  and  cop})er 
salts.  This  is  called  })ositive  chemotaxis.  The  opposite  is  negative 
chemotaxis. 

Toxins  are  negatively  chemotactic,  and  when  bacteria  produce 
much  toxin  phagocytosis  and  suppuration  is  lessened,^  e.  g.,  in 
stre})tococcus  infection.  jNIany  other  bacterial  products  and  bacterial 
proteins  are  positively  chemotactic,  and  when  they  are  produced  in 
place  of  much  toxin  phagocytosis  is  increased,  and  the  bacteria, 
if  few,  are  coincidently  destroyed  by  the  alexins  and  taken  up   by 


'  Cellular  Toxins. 

3  Stengel,  A  Text-book  of  Patl 


^  J.  J.  McKenzie,  Dominion  Dental  Journal. 


52      MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

the  phagocytes  with  resokition,  or,  if  the  bacteria  be  numerous, 
suppuration  is  increased  and  the  bacteria  expelled  as  a  protection  to 
the  body. 

If  the  combined  local  forces  be  incompetent  to  kill  out  the  infecting 
organisms,  the  local  infection  spreads  until  limited  or  the  patient  dies; 
or  a  metastasis  may  occur,  in  which  case  the  process  is  practically 
repeated  in  another  locality. 


IMMUNITY. 

Immunity  is  the  opposite  of  predisposition,  and  may  be  defined  as 
such  a  condition  of  the  local  fluids,  the  blood,  or  the  body  cells,  that 
innoculation  with  bacteria  or  bacterial  products  has  no  injurious 
effects. 

There  is  also  some  relative  immunity  to  non-infectious  diseases,  e.  g., 
females  to  hemorrhagic  diathesis.  Immunity  to  infective  agencies  may 
be  natural  or  acquired. 

Natural  Immunity. — This  is  usually  an  inheritance  from  immune 
ancestors  of  a  type  of  tissue  anatomy  and  physiology,  or  a  peculiar 
substance  in  the  blood,  etc. 

Typical  examples  of  this  kind  of  immunity  are  those  of  the  rat  to 
diphtheria;  man  to  rinderpest;  lower  animals  to  syphilis;  the  negro 
to  yellow  fever  (though  he  is  susceptible  to  smallpox);  the  hog  to 
snake  venom,  etc. 

Natural  immunity  may  change  to  susceptibility  through  some 
change  in  the  systemic  condition.  Thus,  two  students  attending  a 
scarlet-fever  ward  for  months  became  susceptible  through  the  effects 
of  a  long  walk  and  hunger;  both  took  the  fever,  one  dying. ^ 

Rats,  run  in  a  wheel  until  exhausted,  were  successfully  innoculated 
with  anthrax  bacilli,  to  which  they  are  normally  insusceptible. 

Natural  immunity  may,  therefore,  fail  upon  severe  test,  and  survival 
of  the  test  is  the  only  certain  assurance.  This  natural  immunity  may 
be  of  two  kinds: 

1.  Natural  toxin  immunity,  e.  g.,  hog  to  snake  venom. 

2.  Natural  bacterial  immunity,  e.  g.,  negro  to  yellow  fever. 
Acquired  Immunity. — This  is  of  two  kinds: 

1 .  Acquired  toxin  immunity. 

2.  Acquired  bacterial  immunity. 

'  Green,  Pathology  and  Morbid  Anatomy. 


IMMUNITY  53 

Acquired  Toxin  Immunity. — Toxin  immunity  may  be  acquired 
in  two  ways: 

1.  By  the  injection  of  small  doses  of  toxins  at  intervals  until  no 
reaction  results.  The  horse  is  so  immunized  in  diphtheria  antitoxin 
production. 

2.  By  the  injection  into  man  or  animals  of  serum  containing  anti- 
toxin produced  by  method  No.  1.  The  former  is  an  active  immunity; 
the  latter  passive. 

Acquired  Bacterial  Immunity. — Immunity  to  bacterial  innocula- 
tion  may  be  acquired  in  several  ways: 

1.  Naturally  through  having  had  an  attack  of  the  particular  specific 
disease,  thus,  as  a  rule,  measles,  smallpox,  syphilis,  yellow  fever,  and 
many  other  infectious  diseases  produce  bodies  which  remain  in  the 
blood  and  render  the  individual  immune  to  a  second  attack,  though 
in  some  cases  this  immunity  is  lost.  The  child  of  a  syphilitic  mother 
is  often  rendered  immune  to  syphilis  though  apparently  healthy, 
and  cannot  be  subsequently  infected  by  her  (Profeta's  law);  also, 
the  mother  of  a  syphilitic  child  may  show  no  symptoms  of  the  disease 
and  be  immune  to  it  (Colics'  law).  The  toxin  is,  in  both  cases, 
absorbed  through  the  placenta,  immunizing  the  child  or  mother,  as 
the  case  may  be. 

2.  Artificially  through  the  injection  into  the  body  of  attenuated 
cultures  of  bacteria,  grown  through  several  generations  under  unfavor- 
able conditions,  wdiereby  their  virulence  is  lost:  a  mild  immunizing 
attack  ensues.  Thus,  in  rabies,  or,  rather,  for  prevention  of  rabies,  after 
the  bite  of  an  animal  suffering  from  it,  accurately  graduated  doses  of 
emulsions  of  the  spinal  cord  of  rabbits,  dried  for  varying  periods  to 
produce  accurately  degenerated  rabies  germs,  are  injected  into  man, 
preventing  the  development  of  the  germs  introduced  by  the  bite.  The 
emidsion  of  older  cords  are  injected  first,  then  those  of  younger  cords 
(dried  for  a  shorter  time). 

3.  Artificially  by  the  injection  of  graduated  doses  of  toxins,  pro- 
duced in  a  saprophytic  medium  by  the  specific  bacterium,  all  bacteria 
being  filtered  out. 

The  horse  is  so  treated  in  the  production  of  diphtheria  antitoxin 
for  use  in  the  diphtheria  of  man. 

4.  Artificially  by  the  injection  of  the  serum  of  animals  inununized 
by  method  No.  3,  which  serum  contains  a  substance  antagonistic  to 
the  specific  toxin  and  known  as  an  antitoxin,  also,  possibly,  a  substance 
antagonistic  to  the  bacteria  producing  the  toxin.    Thus,  the  injection 


54       MICROORGANISMS  AS  EXCITIXG  CAUSES  OF  DISEASE 


of  horse  serum  containing  antitoxin  of  diphtheria  produced  by  method 
No.  3  into  a  diphtheric  patient  aborts  the  disease  by  antagonizing 
both  the  bacteria  and  its  toxin.  Injection  into  the  attending  nurse 
produces  immunity  to  the  disease. 

The  methods  1,  2,  and  3  produce  a  much  more  lasting  immunity, 
as  the  antagonizing  substance  is  the  result  of  cell  reaction  on  the  part 
of  the  individual,  and  is  called  active  immunity;  that  produced  by 
method  No.  4  is  passive,  because  not  produced  by  cell  reaction  but 
directly  introduced  into  the  blood,  and  is  much  less  lasting. 

The  various  forms  of  immunity  are  explainable  by  the  now  gener- 
ally accepted  theory  of  Ehrlich  known  as  the  lateral  chain  theory. 


Fig.  26 


Fig.  27 


-4,  pomplement;  B,  amboceptor; 
C,  leceptor;  D,  part  of  cell. 


Cell    with    different   kinds   of    receptors:  C,  receptors. 


Ehrlich's  Lateral  Chain  Theory. — ^This  theory  is  based  upon  certain 
demonstrated  facts  and  upon  the  supposition  that  each  cell  is  composed 
of  a  complex  nucleus  made  up  of  groups  of  molecules  in  turn  composed 
of  aggregations  or  groups  of  atoms  and  surrounded  by  side  groups  of 
atoms  (molecules),  which  compose  the  cell  protoplasm.  Each  atom 
group  is  supposed  to  have  its  own  chemical  affinity  for  food  elements, 
poisons,  etc.,  as  shown  by  the  selective  affinity  of  drugs. 

These  chemical  atom  groups,  therefore,  have  a  receptive  function 
and  are  called  receptors  (on  the  cell).  Other  groups  have  a  ferment- 
ative action  and  chemically  change  the  substances  presented:  these 
are  called  zymophorous  atom  groups. 

Each  toxin  molecule  has  an  affinity  for  some  cell  receptors,  otherwise 
no  effect  is  produced  })y  it.  (Snake  venom  has  no  effect  upon  the 
hog.) 


IMMUNITY 


55 


The  receptor  is  considered  to  possess  a  group  of  atoms  suited  to  a 
prehending  action,  whereby  it  combines  with  the  toxin  molecule  (or 
food  molecule  in  nutrition),  which  possesses  a  similar  combining  group 
of  atoms.  In  each  these  are  termed  the  haptophorous  group.  The 
toxin  molecule  is  capable  of  inflicting  injury  upon  or  stimulating  cell 
action,  as  shown  in  the  case  of  tetanus,  in  which  tonic  muscular  con- 
tractions are  excited.  The  group  of  atoms  in  the  toxin  molecule, 
which  accomplishes  this,  is  termed  the  toxophorous  group  (Fig.  27j. 

That  the  body  cells  neutralize  the  toxin  if  not  in  overwhelming 
fjuantity,  is  siiown  by  the  experiment  of  Eln-lich,  in  which  a  mixture 
of  brain  emulsion  and  tetanus  toxin  was  inert  when  injected  into  a 


Fig.  28 


Fig.  29 


Showing  separation  of   antitoxins,  and  com- 
binations of  toxins  with  free   antitoxins. 


Showing  the  action  of  anticomple- 
ment:  A,  complement;  B,  intermediary 
body;  C,  receptor;  D,  cell;  E,  antieom- 
plement. 


susceptible  animal.    Therefore,  a  zymophorous  group  of  atoms  is  said 
to  exist  in  the  cell  or  its  receptor. 

The  Theory  of  Toxin  Immunity. — The  toxin  produced  during  an 
infective  disease,  such  as  diphtiieria,  and  floating  in  the  blood,  presents 
itself  to  cells,  for  some  receptors  of  which  it  has  an  afhnity.  The  hap- 
tophorous atom  group  of  its  molecule  joins  with  the  haptophorous  atom 
group  of  the  receptor.  The  toxophorous  group  exerts  its  action  upon 
the  receptor  and  is  neutralized  by  the  zymophorous  group  of  the  latter 
unless  the  toxin  is  in  too  great  quantity.  The  cell,  in  case  of  injury, 
repairs  itself  by  forming  an  excess  of  the  particular  kind  of  receptors 
having  affinity  for  the  particular  toxin.  These  receptors  l)ecome 
detached  and  float  in  the  blood,  and  there  have  the  same  afiinitv  for 


56       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

the  toxin.  These  are  called  receptors  in  the  blood  and  constitute  what 
is  known  as  antitoxin.  They  are  known  to  be  formed  by  the  body 
cells  and  not  by  the  blood,  as  they  have  been  found  in  the  tissue 
juices  of  blood-making  organs  immediately  after  the  introduction  of 
toxin,  while  at  the  same  time  not  found  in  the  blood,  though  they 
afterward  appear,  as  might  be  expected  (Fig.  28) . 

The  antitoxin  receptor  (with  affinity  for  the  toxin  molecule)  has 
an  haptophorous  atom  group  which  combines  with  the  haptophorous 
group  of  the  toxin  molecule,  which,  having  found  its  affinity  in  the 
blood  is  satisfied,  does  not  further  affect  the  cells  proper,  and  thus 
cell  injury  is  prevented.  This  occurs  in  each  case  of  diphtheria,  and 
probably  recovery  or  death  is  dependent  upon  the  ability  of  the  body 
cells  to  furnish  antitoxin  sufficient  to  antagonize  the  toxin  and 
another  body  to  be  described  which  antagonizes  the  bacteria. 

In  the  case  of  serum  therapeutics,  the  horse  is  compelled  by  method 
No.  3  to  form  these  antagonizing  substances,  and  the  serum  is  then 
injected  into  the  individual  suffering  an  attack  or  threatened,  thus 
furnishing  him  ready  made  the  antagonizing  substances  (antitoxin, 
etc.).  A  special  antitoxin  is  supposed  to  be  formed  for  each  kind 
of  toxin.  In  old  sera  the  toxin  undergoes  a  chemical  change  into 
toxoid,  and  the  injection  of  this  causes  an  increase  of  receptors  on 
the  cell  and  thus  renders  the  animal  more  susceptible  to  the  action  of 
the  toxin. 

Toxone  is  a  third  body  produced  by  the  bacteria  which  has  some 
affinity  for  antitoxin,  but  the  combination  is  still  somwhat  toxic, 
and  in  diphtheria  is  credited  with  the  production  of  postdiphtheric 
paralysis. 

The  Theory  of  Acquired  Bacterial  Immunity. — ^When  bacteria  enters 
the  tissue  of  an  animal  by  inoculation  and  are  not  destroyed  by  the 
alexins  and  phagocytes,  they  develop  and  produce  toxins  and  may 
themselves  enter  the  blood.  A  reaction  of  the  body  cells  occurs,  as 
shown  by  fever,  and  not  only  antitoxin  but  another  body  is  produced 
by  the  cells,  which,  with  the  aid  of  another  substance  called  comple- 
ment, is  capable  of  destroying  the  particular  bacterium  causing 
the  infection.  This  body  is  another  form  of  receptor  having  two 
haptophorous  groups  by  which  it  links  the  complement  with  the  re- 
ceptor of  the  bacterium,  and  thus  enables  the  complement  to  destroy 
the  bacterium  through  its  zymophorous  atom  group.  The  doubly 
haptophorous  receptor  is  called  from  this  fact  the  amboceptor  (also 
intermediary  or  immune  body)   (Fig.  26). 


IMMUNITY  57 

The  complement  is  probably  produced  bv  the  leukocytes  and  is 
classed  among  the  alexins.  As  stated,  it  has  a  zymophorous  atom 
group,  and  also  has  an  haptophorous  atom  group  with  which  it  joins 
the  amboceptor.  The  complement  is  destroyed  at  55°  C.  (is  ther- 
molabile).  The  amboceptor  requires  a  higher  heat  (is  "thermo- 
stabile) ;  a  different  amboceptor  is  probably  formed  for  each  variety 
of  bacterium. 

In  natural  bacterial  innnunity  it  is  thought  that  some  of  the  ambo- 
ceptors are  inherited  from  immune  ancestors,  and  that  they  exist 
together  with  complement  in  the  blood  ready  to  act. 

Agglutination. — When  body  cells  react  to  infection,  and  attempt  to 
or  effect  immunity,  the  blood  plasma  acquires  the  property  of  clumping 
the  bacteria  together,  and  they  settle  to  the  bottom  of  a  test  serum, 
leaving  the  fluid  clear.  It  is  supposed  to  be  exhibited  only  toward  the 
bacterium  causing  the  infection,  but  experimentally  out  of  the  body 
{in  vitro)  others  are  sometimes  affected. 

The  substance  producing  agglutination  evidently  exists  in  blood  as 
the  result  of  cell  reaction.  It  is  of  the  nature  of  liberated  amboceptors, 
but  has  a  zymophorous  group.  It  therefore  acts  by  combining  by 
an  haptophorous  group  and  acting  through  a  zymophorous  group. 

The  reaction  is  useful  in  making  a  diagnosis  of  the  kind  of  existing 
infection.  Thus,  if  typhoid  bacillus  be  suspected  as  a  cause  of  disease 
present  and  be  the  cause,  the  blood  serum  drawn  will  agglutinate 
living  typhoid  bacilli  placed  in  it.  Snake  venom  possesses  agglutinins 
which  clump  and  destroy  red  corpuscles. 

Opsonins. — Certain  substances  among  the  alexins  were  found  to 
render  bacteria  more  subject  to  phagocytosis.  Wright  has  called  these 
opsonins.  They  have  an  haptophorous  group  joining  the  bacteria  and 
a  zymophorous  group  acting  on  them.  They  thus  degenerate  them. 
They  differ  from  bactericidal  substance  because  they  do  not  neces- 
sarily destroy  them.  This  is  completed  in  the  leukocytes.  The 
opsonins  can  be  increased  by  proper  therapy  and  can  be  diminished 
by  debilitating  conditions.  The  information  gained  by  a  test  of  the 
serum  of  a  patient  is  called  by  Wright  the  opsonic  index.  It  is  useful 
in  estimating  the  power  of  phagocytosis  in  individuals,  especially  in 
tuberculosis. 

The  Reaction  of  the  Blood. — According  to  Michaels^  (following 
Gautrelet),  individuals  in  whom  the  oxidations  are  below  normal,  and 
who  have  a  tendency  to  arthritic  diseases  because  of  an  excess  of  the 

'  Sialosemiology. 


58       MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

acid  constituents  or  waste  products  in  the  body  fluids,  are  denom- 
inated hyperacid  individuals.  The  hypoacid  have  oxidations  above 
the  normal,  together  with  a  superabundance  of  saline  chlorides;  and 
these  he  regards  as  more  subject  to  infection.  There  are  three  ways 
in  which  the  predisposition  of  the  hypoacid  might  be  accounted  for : 

1.  The  increased  amount  of  alkaline  elements  may  permit  an  alka- 
line reaction  of  the  blood,  rendering  it  favorable  to  bacteria  as  a  culture 
medium. 

2.  The  systemic  change  may  introduce  a  substance  into  the  blood 
which  is  a  suitable  pabulum  for  the  bacteria  (according  to  Kirk^ 
this  occurs  in  the  saliva  in  those  susceptible  to  caries). 

3.  Certain  immunizing  substances,  opsonins,  alexins,  etc.,  may 
fail  to  be  formed. 

Per  contra,  the  hyperacid  may  be  immune  for  opposite  reasons. 
Whether  this  be  a  rational  explanation  or  not,  it  is  certainly  shown  by 
Wright  that  therapy  will  increase  the  opsonic  index,  and  it  may  be 
that  in  the  hyperacid  the  continuous  cell  irritation  by  the  acid  ele- 
ments, as  CO2  uric  acid,  etc.,  may  cause  a  tissue  reaction  increasing 
alexin  or  opsonic  power. 


EXTERNAL  ANTIBACTERIAL  INFLUENCES. 

Many  chemical  substances  and  physical  forces  prevent  the  growth 
and  reproduction  of  bacteria  without  necessarily  killing  them;  these 
are  called  antiseptics;  a  weak  solution  of  boric  acid  is  an  example, 
agitation  is  another,  dryness  another.  Other  substances  or  forces 
kill  the  bacteria  after  an  exposure  to  their  influence  for  a  sufficient 
length  of  time;  these  are  germicides — e.  ^.,  a  1  to  1000  solution  of  mer- 
curic chloride  in  water,  boiling  water,  or  streaming  steam;  light  for 
some  bacteria.  Other  substances  destroy  both  the  bacteria  and  their 
products;  these  are  disinfectants — e.  g.,  sodium  dioxide  or  other 
substances  liberating  nascent  oxygen. 

1  Dental  Brief,  1907. 


CHAPTER    IV. 

DISTURBANCES  OF  NUTRITION. 

Disorders  of  nutrition  are  of  three  classes:  (1)  due  to  an  excess  of 
nutritive  material  of  all  classes,  or  of  one  class;  (2)  due  to  a  deficiency 
of  nutritive  material,  active  or  relative;  (3)  due  to  the  presence  in 
the  blood  of  material  which,  instead  of  serving  the  purpose  of  metab- 
olism, disturbs  it;  (4)  an  inability  of  the  cells  to  appropriate  a  proper 
quantity  and  quality  of  food. 

EXCESS  OF  NUTRITION.    HYPERNUTRITION. 

An  excess  of  nutrition  may  be  either  general  or  local.  If  local, 
it  is  associated  with  an  overfulness  of  the  bloodvessels  (hyperemia). 
If  the  individual  possess  a  general  richness  of  blood,  he  is  said  to  be 
plethoric.  Sthenic  plethora  is  such  a  richness  associated  with  activity 
of  the  circulation  and  a  consequent  increase  of  the  vital  processes 
due  to  plentiful  cell  nutrition,  and  with  an  active  repair  of  even  exces- 
sive waste  of  cell  protoplasm. 

In  asthenic  plethora,  on  the  contrary,  the  individual  is  full  blooded, 
but  the  circidation  is  sluggish;  waste  products  are  probably  accumu- 
lated in  the  l)loofl  and  the  vital  processes  are  sluggish  in  consequence. 
Instead  of  the  rich  color  and  active  movements  associated  with  sthenic 
plethora,  the  asthenic  have  a  })urpllsli  aj)pearance  and  the  movements 
are  more  labored. 

Local  Hypernutrition. — An  increased  stimulation  of  the  nerves  of 
a  part  invites  mure  blooil  to  it,  which  within  certain  limits  increases 
the  nutrition  to  the  cells  of  the  part.  This  results  in  increased  irri- 
tability, contractility,  and  general  functional  activity  of  the  function- 
ating cells.  If  this  be  maintained,  the  cells  grow  or  multiply,  or  both, 
and  the  part  is  enlarged  and  capal)le  of  an  increased  amount  of  work. 

Stimulation  beyond  this  point  causes  irritation  or  overstimulation 
of  cells,  and  the  vital  processes  become  fretful;  incomplete  chemical 
changes    occur    in    the    cells,    and    the    functional   activity   is   di.s- 


60  DISTURBANCES  OF  NUTRITION 

ordered.     The  cells  are  wearied,  and  if  the  overstimulation  be  con- 
tinued paralysis  from  overwork  results. 

Hypertrophy. — Though  strictly  meaning  an  excess  of  nutrition, 
this  term  signifies  an  increase  in  size  of  a  part  as  the  result  of  • 
stimulation  and  destruction,  with  a  compensatory  rebuilding  of 
cell  material  in  excess  (a  cell  hyperplasia)  (Weigert^).  The  new- 
growth  must  be  practically  normal  in  structure.  As  a  rule,  both  the 
size  (simple  hypertrophy)  and  number  of  the  cells  (numerical 
hj'pertrophy  or  hyperplasia)  are  increased.  The  caliber  of  the 
bloodvessels  is  increased  to  comply  with  the  stimulus  to  their  con- 
trolling nerves — the  vasomotors.  Hypertrophy  is  frequently  exhibited 
in  tissues  subjected  to  an  unusual  amount  of  work  short  of  marked 
fatigue.  An  increase  in  its  function  occurs;  its  capacity  for  work 
becomes  greater,  and  if  the  strong  stimulus  (mild  irritation)  imphed 
be  continued  the  cells  increase  in  size  and  it  may  be  in  number,  all 
three  phases  of  the  expenditure  of  an  increase  of  vital  energy  being 
represented — afunctional,  nutritive,  and  reproductive.  If  the  heart 
be  subjected  to  an  increase  in  the  strain  ordinarily  brought  upon  it, 
an  increase  in  the  volume  of  the  muscular  fibers  follows,  causing  hyper- 
trophy of  the  walls.  The  same  is  true  of  the  muscles  of  the  gravid 
uterus,  in  which  the  cells  increase  to  many  times  their  normal  length. 
^Tien  one  organ,  as  a  kidney,  takes  up  alone  the  work  usually  per- 
formed by  two  it  increases  in  size  (hypertrophies).  This  is  called  com- 
pensatory hypertrophy.  It  may  occur  in  an  organ  which  endeavors 
to  supply  the  deficient  function  in  another  organ  of  different  sort. 
Hypertrophy  also  occurs  in  many  inflammatory  conditions,  and  is  due 
to  the  area  of  hyperemia  surrounding  every  focus  of  inflammation. 
Thus  the  epithelium  about  the  edges  of  an  ulcer  may  thicken  or  new 
bone  may  be  formed  about  an  area  of  inflamed  bone  tissue  or  perios- 
teum. The  bone  tissue  may  become  more  compact,  a  condition 
termed  sclerosis  of  bone,  as  it  results  in  the  formation  of  formed 
(intercellular)  tissue  at  the  expense  of  the  cellular  elements. 

The  removal  of  an  accustomed  resistance  often  produces  an  irrita- 
tion resulting  in  mild  hyperemia,  and  thickening  or  hypertrophy 
results — e.  g.,  non-occlusion  of  teeth  frequently  produces  hyper- 
cementosis. 

A  form  of  cellular  hypertrophy  appears  to  occur  in  certain  leuko- 
cytes, resulting  in  the  formation  of  a  multinucleated  cell  or  "giant 
cell." 

'  See  Abbott's  Principles  of  Bacteriology,  p.  601,  for  an  amijjification  of  this  idea. 


EXCESS  OF  NUTRITIOX.     HYPERXUTRITIOX  61 

Under  irritation  the  nucleus  subdivides,  but  the  cell  body  fails  of 
division,  and  instead  of  complete  reproduction  a  large  cell  with  many 
nuclei  is  formed  (Fig.  30).  These  giant  cells  appear  where  tissue  is 
to  be  removed,  as  in  the  case  of  aseptic  foreign  bodies  or  the  roots  of 
deciduous  or  even  of  permanent  teeth.  (See  Resorption  of  Temporary 
Teeth.)  An  hypertrophy  or  excessive  development  may  occur  during 
intra-uterine  life  and  is  spoken  of  as  congenital  hypertrophy.  A  low 
grade  of  inflammation  may  lead  to  a  numerical  hypertrophy,  as  in  the 
case  of  hypertrophy  of  the  dental  pulp  (which  see). 

Hyperplasia. — Hyperplasia,  sometimes  called  false  hypertrophy,  is 
an  increase  in  size  partly  due  to  an  increase  in  the  number  of  the  cells, 
though  the  individual  cells  may  be  smaller  than  normal.  It  occurs 
mostly  in  the  connective  tissues,  though  it  ordinarily  plays  a  part  in 
most  hypertrophies.  The  part  is  usually  asymmetrical.  Examples: 
elephantiasis — or  hyperplasia  of  the  dental  pulp. 

Fig.    30 


d 

Dog's  hair  encapsulated  in  subcutaneous  tissue:  a,  hair;  6,  fibrous  tissue;  c,  proliferating 
granulation  tissue;  d,  giant  cells.  Preparation  hardened  in  alcohol,  stained  with  Bismarck 
brown,  and  mounted  in  Canada  balsam.      X  OG.   (Ziegler.) 

Cyst  and  Tumor  Formation. — A  cyst  is  an  enlargement  contain- 
ing a  cavity  which  in  turn  contains  liquid,  gelatinous,  or  pultaceous 
material,  about  which  is  a  capsule  condensed  from  the  surrounding 
structures.  The  accumulation  of  the  fluid  or  semifluid  contents 
produces  the  enlargement  of  the  part  even  if  bony  (Fig.  .31). 

They  difi'er  from  tumors  in  being  strictly  localized,  though  they 
may  be  large,  and  in  their  generally  benign  character,  though  tumors 
may  at  times  have  a  cystic  character. 

Cysts  may  be  formed  by  the  retention,  secretion,  or  extravasation 
of  fluid  in  several  ways:  (1)  By  the  retention  of  normal  secretion  of 
a  gland  owing  to  the  obstruction  of  its  duct — e.  g.,  ranula.  These 
are  called  retention  cysts.  (2)  By  abnormal  secretion  into  ductless 
cavities — e.  g.,  bursae  (exudation  cysts).  (3)  By  the  extravasation 
of  blood  into  a  ductless  cavity  (extravasation  cyst).  (4)  Independ- 
ently in  tissue  as  a  result  of  mucoid  or  fatty  changes  or  liquefaction 


62 


DISTURBANCES  OF  NUTRITION 


necrosis,  the  surrounding  tissue  becoming  condensed  into  a  capsule 
(liquefaction  cysts).  (5)  Independently  as  a  collection  of  fluid  in 
connective-tissue  spaces,  which  enlarge  and  fill.  The  surrounding 
tissue  condenses  into  a  cyst  wall.  (6)  Independently  as  a  result  of 
chronic  irritation  by  foreign  bodies,  extra vasated  blood,  or  parasites, 
as  in  dentigerous  cysts^  (Fig.  31).  Cysts  may  have  but  one  cavity 
(simple  cysts)  or  have  numerous  intercommunicating  cavities  known 
as  loculi  (compound  or  multilocular  cysts).  Forming  within  bony 
walls,  these  may  be  largely  distended  and  the  walls  are  usually  thin. 
Dentigerous  and  other  cysts  are  usually  lined  by  epithelium  peculiar 
to  the  part.     The  explanation  of  Malassez,  that  epithelial  remnants 


Cyst  of  the  lower  jaw,  having  its  origin  about  an  undeveloped  tooth      (Garretson.) 

(as  the  enamel  organs)  develop  forcing  the  connective-tissue  elements 
outward  as  a  covering  to  them,  is  probably  the  correct  one.  Mean- 
while, fatty  degeneration  of  developed  epithelium  and  the  collection 
of  fluid  account  for  the  fluid  or  pultaceous  character  of  the  cyst 
contents.  This  proliferation  of  epithelial  remnants  is  well  proved  by 
the  development  of  epithelial  products  in  the  interior  of  dermoid 
cysts. 

Dermoid  cysts  are  cystic  tumors  of  widely  varying  sizes  found  in 
various  parts,  such  as  the  ovary,  neck,  base  of  brain,  orbit,  etc.  They 
contain  fatty  and  epithelial  debris,  and  are  lined  with  epithelium, 
outside  of  which  is  a  corium  with  its  papillae,  and  outside  of  this 
su})cutaneous  adipose  tissue.     The  whole  is  enclosed  in  a  fibrous 

1  Green. 


EXCESS  OF  NUTRITION.     HYPERNUTRITION.  63 

capsule  of  coniiectivo  tissue.  The  epithelial  lining  may  contain  and 
develop  the  characteristically  dermoid  structures,  hair,  teeth,  sebaceous 
and  sweat  glands  (Fig.  34). 

Broomeir  states  that  the  hair  is  often  several  feet  long,  usually  of 
a  light-brown  color,  regardless  of  the  color  on  the  outside  of  the 
bodv,  and  becomes  white  as  age  whitens  the  outside  hair,  and  is 
usually  absent  in  dermoids  in  bald  persons.  Hair  follicles  are 
present. 

Fio.    32 


Li)nKitU(linal  sertion  <if  a  tooth  from  an  ovarian  cyst:  n,  h,  d,  tissue  filling  absorption  cavities; 
c,   narrow  hand  of  connective  tissue  through  which    the    organ  a  received  its  nourishment; 

(/,  aljsorption  of  enamel.      (Miller.) 

He  states  that  "Dermoids  of  tlie  mouth  are  usually  found  in  tlic  h.ard 
and  soft  palates,  infrecjuently  in  the  former,  but  when  found  are  com- 
plicated, while  the  more  frequently  found  in  the  soft  palate  are 
sim])ler.  In  these  situations  they  range  from  the  size  of  a  pea  to  that 
of  a  hen's  egg,  the  larger  Ix'ing  pendulous.  They  are  also  found  on 
the  floor  of  the  mouth  and  dorsum  of  the  tongue. 

"The  cementum  is  usually  absent  or  but  slightly  developed. 

"The  teeth  range  in  shape  from  the  simple  cone  to  multicusped  com- 
plex forms,  the  crowns  of  the  same  being  well  fornuMl.     'Vhv  roots  are 

»  Dental  Cosmos,  1905. 


64 


DISTURBANCES  OF  NUTRITION 


usually  not  fully  calcified  or  developed,  or,  perhaps,  partly  developed. 
A  follicular  wall  is  present.     The  enamel  may  be  smooth  or  pitted. 

"Radicular  odontomes  evidenced  by  tumor-like  growths  on  roots 
are  due  to  aberration  of  the  dentinal  germ.  The  pulp  canal  was 
always  present  in  cases  examined.  Fusion  of  teeth  has  occurred  in 
these  cysts.  In  histology  the  teeth  are  similar  to  ordinary  teeth, 
with  some  slight  aberration  due  to  the  peculiar  condition." 

Miller^  states  that  the  cystic  contents  include  fatty  acid,  oxalic 
acid,  large  quantities  of  tyrosin  and  leucin,  which  substances  furnish 


Fig.  33 


Absorption  tissue,  from  cavity  a  in  Fig.  32. 

the  acid  for  the  decalcification  of  teeth  occasionally  found,  but  that 
no  bacterial  action,  such  as  occurs  in  the  second  stage  of  dental 
caries,  could  be  found.  He  stated  that  in  those  teeth  having  living 
living  pulps  transparency  might  be  found. 

Tumors.— A  tumor  is  a  new-growth  conforming  to  a  degree  to  the 
normal  histology  of  a  part,  but  having  no  physiological  function  and 
no  typical  limit  of  growth.  They  are  classed  as  benign  or  malignant, 
accordingly  as  they  are  strictly  localized  and  comparatively  harmless, 

'  Dental  Cosmos,  1905. 


EXCESS  OF  NUTRITIOX.      IIYPERXVTRITIOS  65 

or  tentl  to  sap  vitality  and  to  s})rea(l  dangerously,  or  to  be  transferred 
to  other  localities  (metastasis.) 

The  growdi  of  a  tumor  is  attended  by  a  sapping  of  the  vitality  of  a 
sufferer — the  degree  of  the  debility  produced  being  apparently  in 
direct  ratio  to  the  size  and  the  rapidity  of  the  growth.  Besides  the  size 
and  the  rapidity  of  development  of  individual  tumors,  another  element 
determines  their  malignancy,  their  position,  and,  furthermore,  their 
occurrence  in  other  parts,  resulting  in  multiple  tumor  formation.  A 
tumor  victim  acquires  a  j)('culiar  appearance — a  cachexia  whose  inten- 
sity and  rai)idity  of  advance  are  directly  dependent  upon  the  degree  of 


Portion  of  a  wall  of  an  ovarian  dermoid  cyst:  o,  wall  of  the  cyst;  b,  projecting  portion 
made  up  of  fatty  and  cutaneous  tissue;  c,  hairs;  d,  teeth.     (Ziegler.) 

malignancy,  and  produced  by  the  effects  upon  general  mitrition  of  the 
toxic  substances  entering  the  circulation. 

Tumors  introduce  no  new  form  of  tissue  element;  they  are  repro- 
ductions of  the  cells  of  the  tissues  of  the  body.     They  may  have  the 
same  cell  formation  as  the  tissue  from  which  they  spring,  and  are  then 
called  homologous  tumors;  or  they  may  have  a  different  histological 
5 


66  DISTURBANCES  OF  NUTRITION 

structure  from  the  tissue  in  which  they  are  found,  being  then  called 
heterologous  tumors.  For  example,  a  bony  tumor  growing  from  bone 
would  be  homologous;  a  cartilaginous  tumor  growing  from  gland  tissue 
would  be  heterologous. 

Causes. — ^The  causes  of  tumor  formation  are  unknown;  it  has  been 
believed  that  their  growth  is  due  to  parasites,  especially  the  protozoa; 
this,  however,  has  not  been  proved.  A  certain  proportion  of  tumor 
formations,  7  to  14  per  cent.,^  appear  to  be  caused  by  traumatic  injury; 
as,  for  example,  in  cases  of  mammary  tumor,  a  history  of  a  blow  or 
fall  may  be  at  times  obtained. 

Long-continued,  sluggish  inflammation  appears  to  be  causative  of 
tumor  formation  in  an  unknown  percentage  of  cases.  A  chronic  irrita- 
tion of  certain  portions  of  the  body,  such  as  the  junction  between  the 
mucous  and  skin  surfaces  of  the  lip,  the  sides  of  the  tongue,  etc.,  is  a 
frequent  antecedent  to  their  formation.  Ziegler  gives  a  reasonable 
explanation  of  the  origin  of  certain  epithelial  tumors  in  organs  which 
are  undergoing  atrophy;  for  example,  in  advanced  age  the  connective 
tissue  of  the  body  is  undergoing  atrophy  and  there  is  relaxation  of  its 
strata;  the  epithelium  of  the  surface  (or  of  glands),  still  possessed  of  its 
power  of  reproduction,  proliferates  and  invades  the  connective  tissue, 
producing  cancer. 

Cohnheim  advanced  the  theory  that  embryonic  remnants  are 
included  in  the  tissues  and  in  time  reassert  their  proliferative  powers. 

Tumor  formation  consists  in  the  reproduction  of  the  cells  of  one  or 
more  tissues,  and  in  the  growth  thus  formed  bloodvessels  are  developed. 
Tumors  do  not  contain  nerves,  though  they  may  develop  in  nervous 
tissue. 

"The  bloodvessels  of  tumors  have  comparatively  fragile  and  poorly 
developed  walls.  In  the  malignant  growths  or  rapidly  developing 
tumors  of  any  sort  the  vessels  are  mere  spaces  between  the  tumor 
cells,  with  little  attempt  at  the  development  of  firm  walls."^ 

About  the  more  slowly  developing  tumors  a  condensation  of  con- 
nective tissue  occurs  in  many  cases,  forming  a  distinct  limiting  wall 
or  capsule  from  which  the  tumor  may  be  enucleated. 

The  two  great  classes  of  tumors,  those  of  mesoblastic  and  those  of 
epiblastic  and  hypoblastic  origin,  may  be  subdivided  into  orders  accord- 
ing to  their  histological  peculiarities. 

'  Ziegler.  2  Stengel,  A  Text-book  of  Pathology. 


EXCESS  OF  NUTRITION.     IIYPERNUTRITIOX 

Class  Oxe.^ 

Tumors  of  Mesoblastic  Tissues 
Order  One. 

Tumors  of  mature  connecjtive  tissue: 
Bony  timiors,  or  osteoma. 
Cartilaginous  tumors,  or  chondroma. 
Fibrous  tumors,  or  fibroma. 
Fatty  tumors,  or  lipoma. 
Mucous  tumors,  or  myxoma. 
Lymphoici-tissue  tumors,  or  lymphoma. 

Order  Two. 

Tumors  of  the  embryonic  connective  tissues: 
The  fleshy  tumors,  or  sarcoma. 

Order  Three. 

Tumors  of  the  higher  tissues: 

Tumors  of  muscle,  or  myoma. 

Tumors  of  nerves,  or  neuroma. 

Tumors  of  bloodvessels,  or  angioma. 

Tumors  of  lymphatic  vessels,  or  lymphangioma. 

Class  Two. 

tumors  of  epiblastic  and  hypoblastic  tissues. 

Papilla  of  skin  and  of  mucous  membrane,  or  papilloma. 

adenoma. 


Tumors  of  glandular  tissue 

carcmoma 

The  tumors  of  epiblastic  and  hypoblastic  type  are  sometimes  called 
epitheliomata,  for  epithelial  tissue  is  their  characteristic  histological 
structure. 

Malignant  tumors  are  found  in  both  of  the  great  classes :  mesoblastic 
and  epiblastic,  and  hypoblastic.  Carcinoma  represents  the  type  of 
malignancy  in  the  epithelial  tumors.  The  sarcomata  are  the  malig- 
nant tumors  of  the  connective-tissue  type. 

Tumors  are  rarely  composed  of  but  one  type  of  tissue;  several  types 
may  be  present,  the  tumor  receiving  its  name  from  the  tissue  predomi- 

1  Modified  from  Green's  Pathology,  p.  148. 


68 


DISTURBANCES  OF  NUTRITION 


nating.  When  the  distinguishing  feature  of  a  tumor  is  two  predomi- 
nating tissues,  the  tumor  is  given  a  compound  name;  as,  for  example, 
when,  in  a  sarcomatous  growth,  numerous  large  multinucleated  cells 
characteristic  of  bone  marrow  are  found,  it  is  called  a  myeloid 
sarcomatous  tumor.  When  fibrous  and  sarcomatous  tissues  are 
distinguishing  features  the  tumor  is  called  a  fibrosarcoma. 

Since  the  malignancy  of  a  tumor  is  due  primarily  to  the  size  and  the 
rapidity  of  its  growth,  it  is  clear  why  sarcomata  are  more  malignant 
than  fibromata,  and  why  some  forms  of  sarcomata  are  more  malignant 
than  others.     To  illustrate: 

Begin  observation  at  the  different  stages  of  connective-tissue  devel- 
opment, when  connective-tissue  cells  have  first  divided,  reproduced; 

Fig.  35 


Porcine  embryo:  rf,  embryonic  connective  tissue  of  mesoblast.     2.5  cm.     X  250. 


the  tissue  produced,  seen  in  granulation  tissue  and  in  the  embryo,  is  at 
the  indifferent  stage,  as  seen  in  section  of  the  embryonic  jaw  (Fig.  35). 
Mesoblastic  cells  at  this  early  period  are  in  an  indifferent  stage;  some 
of  the  cells  shown  in  the  figure  will  form  bloodvessels,  others  will 
become  bone  corpuscles,  others  will  form  fibrous  and  others  muscular 
tissue.  This  structure  has  its  analogue  among  tumors  in  a  soft, 
fleshy,  rapidly  growing  growth,  called  the  round-celled  sarcoma. 
As  cells  expend  their  vital  energy  in  three  ways  (nutritive,  functional, 
and  reproductive  activity),  the  embryonic  cells  of  such  a  growth  may 
expend  their  energy  in  nutrition  (growth),  and  will  then  grow  out  of 
the  indifferent  stage  into  a  more  mature  form  of  connective  tissue, 
the  ultimate  form  of  one  type  being  a  fiber;  an  embryonic  round  cell 
undergoing  a  series  of  form  changes  from  a  small  roimd  cell  to  a  long 
fiber  (Fig.  36).     The  growth  may  cease  at  any  stage  of  this  form 


EXCESS  OF  NUTRITIOX.     JIYPERXUTRITIOX 


m 


change,  tlie  tumor  composed  of  sucli  cell  forms  receiving  a  corre- 
sponding name.  The  embryonic  connective-tissue  tumors,  as  stated, 
are  called  sarcomas,  the  form  of  the  cells  composing  them  giving 
them  a  qualifying  title. 

In  Fig.  3G  are  represented  the  stages  of  development  of  a  connective- 
tissue  fiber  from  a  round  cell.  If  growth  cease  at  stage  1,  and  the  cell 
energy  thereafter   oxpeiid   itself  in  reproduction,  a  rapidly  growing 


Fig.  36 


0    Q 


tumor  composed  of  small  round  cells  is  formed — a  small  round-celled 
sarcoma,  markedly  malignant.  If  the  cells  expend  a  portion  of  energy 
in  growth  of  cell  size,  a  large-celled  sarcoma  is  formed,  less  malignant 
than  the  former.  If  the  cells  expend  a  portion  of  their  energy  in 
forming  intercellular  substance,  reproduction  and  malignancv  are  less 
active.  So  the  spindle  forms,  3  and  4,  represent  less  ra})id  reproduc- 
tion and  lesser  malignancy  than  1  and  2,  although  the  form  4,  which 
should  be  of  less  rapid  reproduction  than  3,  because  of  more  mature 
organization,  is  frequently  more  malignant,  because  less  intercellular 
substance  is  formed,  as  shown  in  Figs.  37  and  38,  the  energy  repre- 


FiG.  37 


Fig    38 


Fig.  37. — Siiuill  spindle-celled  sarcoma  (from  a  tumor  of  the  leg).      X  200. 

Fk;.  38.— Large  spindle-celled  .sarcoma.  To  the  left  the  cells  have  been  separated  by  teasing, 
so  that  their  individual  forms  are  api)arent;  to  the  right  they  are  in  their  natural  state  of 
apposition,  such  as  would  be  seen  in  a  thin  section  of  ttic  tumor.     (N'irchow.) 

.sented  in  that  process  being  u.sed  up  in  reproduction.  The  nearer 
the  approach  to  tli(>  mature  form  ((i.  Fig.  30),  the  .slower  the  growth 
of  the  tumor,  wliicli,  when  composed  of  ti.s.sue  of  this  tvpe,  loses  its 
fleshy  (sarcomatous)  appearance  and  l)ecomes  fibrous,  and  is  hence 
called  a  fibroma. 


70 


DISTURBAXCES  OF  NUTRITION 


^Vhen  a  sarcoma  begins  its  growth  from  bone,  its  histological  char- 
acter is  frequently  modified  (Fig.  39).  It  contains  large  marrow  cells 
which  have  undergone  incomplete  reproduction,  forming  giant  multi- 
nucleated cells;  this  is  a  common  form  of  tumor  emerging  from  the 
sockets  of  teeth.  Some  of  the  cells  of  a  sarcomatous  growth  may  go  on 
to  maturity,  while  others  remain  at  some  stage  of  their  developmental 
career.  INIalignancy  will  be  modified  according  to  the  amount  of 
mature  tissue  formed. 

Epithelial  Tumors. — Growths  arising  from  epiblastic  or  hypoblastic 
tissues  may  be  benign  or  malignant.  What  are  called  the  adenomata 
may  be  taken  as  the  type  of  the  benign  epithelioma;  that  is,  compara- 
tively benign.     They  present  all  of  the  characters  of  typical  glandular 


Fig.  39 


Fig.  40 


'?)<&•    '^ 

©f^^:^ 


Myeloid  epulis  from  lower  jaw:  a,  multi- 
nucleated giant  cells;  b,  oval  cells.  X  265. 
(Pepper.) 


Adenoma  of  the  breast:  a.  group  of  gland- 
ular acini;  b,  fibrous  stroma;  c,  cells  broken 
away  from  their  attaclmient.  X  265. 
(Pepper.) 


tissue:  numerous  acini  lined  with  epithelial  cells  and  surrounded  by 
connective  tissue  (Fig.  40).  Tumors  of  this  type  may  lose  their  com- 
parative benignancy  and  become  of  the  succeeding  epithelial  type. 

Carcinomata. — These  are  growths  arising  from  preexisting  epithe- 
lial tissue,  which  possess  the  characteristics  of  epithelium  developing 
without  limitations  of  a  basement  membrane.  Beginning  upon  a  skin, 
or  mucous  surface,  or  in  a  gland,  the  reproduced  epithelial  cells  are 
not  sharply  marked  off  from  the  connective  tissue  by  a  limiting  mem- 
brane, but,  gaining  entrance  to  the  alveoli  of  connective  tissue,  they 
proliferate  there,  find  their  way  into  lymphatic  vessels  and  lymphatic 
glands,  and  reproduce  epithelial  growths  in  such  places  of  lodge- 
ment, so  that  a  tumor  having  its  origin  in  one  part  may  give  rise 
to  tumors  in  other  parts  of  the  body — metastasis  (Fig.  41). 


DEFICIENCY  OF  NUTRITION.     HYPONUTRITION  71 

Like  the  connective-tissue  tumors,  types  of  carcinoma  differ  as  to 
rapidity  of  growth  in  their  original  situation  and  in  the  degree  of 
transference;  these  factors  determine  their  mahgnancy.  Tumors  of 
the  sarcoma  group  may  also  give  rise  j.^^  ^^ 

to  growths  in  other  parts,  the  tumor  __^  /"p>/?A^^    .^^^ 

cells    being  carried    thence  by   lymph         ^ 
vessels  or  bloodvessels.  /T 

After    a   period,   tumors    frequently     v. 
suffer  such  interference  with  their  nu- 
trition that  degeneration  occurs  in  them. 

After    removal,    some    varieties    of       (-^  -I 

tumors,  both  those  which  infiltrate  sur-        \  , . 

rounding  tissues  and  those  which  are  •^Xc^Trt-^/,^  Of 

metastatic,  show  a  tendency  to  recur-  '       '  "^        ) 

rence;  that  is,  removal  does  not  effect 

a  cure,  and   the  tumor  may  upon   reap-  Section   through  an   aggregation   of 

1  ,  very  young  cancer  cells,   lodged  like 

pearance  assume  another  and  a  more    ^n  embolus  within  a  capillary  of  the 

milicnant  charTCter  liver.       The    parent   growth   was   an 

'^^  _  adenocarcinoma     of      the     stomach. 

Epithelial       tumors       never       become      Preparation    stained    with    hematox- 

tumors  of  the  connective-tissue   type;    ^ '"'         °°'   *■  '^s^""-) 

and,  vice  versa,  connective-tissue  tumors  cannot  become  epithelial 

tumors. 

The  distinction  formed  between  epiblast  and  mesoblast  in  the 
embryo  is  maintained  throughout  life. 


DEFICIENCY  OF  NUTRITION.     HYPONUTRITION. 

If  the  quantity  or  quality  of  the  blood  delivered  to  a  part  be  deficient, 
the  nutrition  of  the  cells  of  the  part  is  impaired.  First,  atony,  a 
lessened  activity  of  the  vital  processes  of  the  part,  occurs.  Cell 
chemistry  is  disordered,  and  waste  products  arc  either  retained  in  or 
about  the  cells. 

The  function  of  the  cells  is  diminished:  if  secretory,  its  secretion 
is  lessened;  if  muscular,  the  cell  has  a  lessened  contractilitv;  the 
relations  between  nutrition  and  waste  are  disturbed;  the  part  becomes 
physiologically  wearied  sooner  than  usual. 

Hypoplasia. — If  the  process  cause  interference  with  the  develop- 
ment of  an  organ,  so  that  it  is  much  below  normal  in  size,  or  the 
development  of  a  part  is  arrested,  whether  from  lack  of  nutrition  or 


ri 


DISTURBANCES  OF  XUTRITIOX 


disturbance  of  developmental  cells,  the  resulting  condition  is  termed 
hypoplasia. 

If  the  parts  fail  entirely  of  development  the  condition  is  called 
agenesia. 

Atrophy. — If  the  process  of  hyponutrition  be  marked,  the  waste  in 
a  previously  normal  part  may  exceed  repair,  and  the  part  affected 
becomes  diminished  in  size  or  atrophied  (Fig.  42  B).  iVtrophy  may- 
be general  or  local.  In  general  atrophy  there  is  a  general  loss  of 
tissue,  due  to  an  excessive  waste  or  faulty  assimilation  of  food  by  the 
tissues.  There  is  a  loss  of  body  weight,  due  first  to  a  loss  of  the  fat, 
later  to  shrinkage  in  the  tissue  cells.  The  shrinkage  in  size  of  the 
tissue  cells  causes  shrinkage  of  the  entire  organ.  The  cells  and  fat 
may  recover  their  size  when  the  faulty  waste  or  assimilation  is 
corrected.     During  atrophy  many  cells  are  lost  through  the  process 

Fig.  42 


Adipose  tissue:  A,  normal:  B,  atrophic,  from  a  case  of  phthisis;   a,  single  fat  cell,  with 
cell  wall,  nucleus,  and  drop  of  fat.      X  300.     (Virchow.) 

of  fatty  degeneration  and  removed  by  the  phagocytes  (leukocytes), 
so  that  atrophy  may,  like  hypertrophy,  be  both  simple  and  numeri- 
cal. An  atrophied  part  is  pale  and  shrunken,  contains  less  fluid, 
and  is  tough  and  fibrous.  At  times  the  fibrous  portion  or  connec- 
tive tissue  may  increase  as  the  cells  diminish  (sclerosis). 

Causes. — General  atrophy  is  caused:^  (1)  By  a  deficient  supply 
of  food  material  delivered  to  the  tissue  cells.  This  may  be  due  to  a 
primary  food  deficiency  or  any  interference  with  its  preparation  for 
absorption  or  with  its  proper  absorption  or  circulation.  (2)  By  ex- 
cessive waste  of  the  ti.ssues  generally,  as  in  fevers,  prolonged  sup- 
puration, etc.  (3)  By  impared  vital  activity  of  the  cells  themselves, 
as  in  senile  conditions. 

Local  atrophy  may  be  caused:  (1)  By  a  lessened  circulation  in 
a  part  due  to  obstruction  of  the  arteries,  veins,  or  capillaries,  as, 
for  example,  by  pressure.     (2)  By  diminished  functional  activity  or 

'  Green. 


Fig.  43 


DEFICIEXCY  OF  NUTRITIOX.     HYPOXUTRITIOX  73 

disuse  of  a  part,  as  in  the  case  of  unused  muscles  or  even  hones. 
Certain  organs  are  atrophied  or  resorbed  as  a  part  of  the  cvcle  of 
life — e.  g.,  the  umbilical  cord,  the  roots  of  deciduous  teeth,  the  thymus 
gland,  the  mammary  glands  after  the  menopause.  (3)  The  loss  of 
nervous  connection  of  a  part  with  the  nerve  centres  controlling  it 
(trophoneurosis),  or  through  interference  with  nervous  centres  having 
trophic  influence  upon  a  part.  (4)  Excessive  fimctional  activity  may 
cause  atrophy  by  ])roducing  a 
degenerative  condition  due  to 
overstimulation. 

Degeneration. — If  cells  have 
reached  the  limit  of  their  life  cycle 
or  have  been  subjected  to  influ- 
ences markedly  disturbing  their 
nutrition,  the  proteids  of  which 
they  are  composed  are  replaced 
by  new  substances  of  somewhat 
obscure  origin,  which  appear  in 
the  parenchymatous  cells,  and 
connective  tissue  markedly  alter- 
ing the  histology  and  producing  a 
pathological  anatomy  peculiar  to 
each  form  of  degeneration.  If  the 
change  is  due  to  chemical  changes 
within  the  tissues,  it  is  a  true  de- 
generation. If  the  new  substance 
enters  the  cell,  it  is  an  infiltration. 


Muscle  fibers  in  simple  atropliy.     (Selunaus.) 

Fatty  Infiltration. — In  this  condition  the  fat  is  found  in  globules 
in  the  cells,  which  globules  tend  to  coalesce.  The  nucleus  may  be 
pushed  aside.  It  is  regarded  as  simply  the  storing  of  fat  in  healthy 
cells,  though  possil)ly  an  infiltration  may  occur  in  a  debilitated  or 
degenerated  (-(^ll  (Fig.  44). 

Fatty  Degeneration. — Fatty  degeneration  is  a  condition  in  which 
the  pathological  accunndation  of  fat  is  found  in  the  substance  of 
cells.  The  cell  a})pears  granular  and  fat-droplets  appear  within  the 
substance  of  the  protoplasm  and  give  a  black  reaction  with  1  per 
cent,  osmic  acid.  These  do  not  tend  to  coalesce,  as  in  the  case  of 
fat  infiltration.  "The  larger  the  amount  of  cell  albumin  replaced  bv 
fat  the  nearer  is  the  whole  cell  to  death"^  (Figs.  4o  and  ■i(\). 


'  t'lieen,  Fathology  and  Morbid  Anatomy. 


74 


DISTURBANCES  OF  NUTRITIOX 


Tliree  theories  are  held  as  to  the  origin  of  the  fat. 

1.  That  the  proteid  of  the  cell  is  changed  to  fat. 

2.  That  fat  is  a  normal  part  of  cell  proteid  and  simply  becomes  more 
visible  because  set  free  through  the  action  of  poison  (such,  as  bacterial 
ferments  or  phosphorus)  acting  upon  the  combination  of  fat  proteids 
in  the  cell.     The  administration  of  phosphorus  to  animals  produces  it. 

3.  That  the  fat  is  infiltrated  from  the  blood,  as  in  fatty  infiltration, 
but  into  diseased  cells.     Thus,  animals  were  poisoned  with  phos- 

FiG.  44  Fig.  45 


Liver  cells  in  various  stages  of  fatty 
accumulation.      X  300.      (Rindfleisch.) 


Fatty  degeneration  of  cells:  a,  from  a  cancer;  b, 
from  the  brain  in  chronic  softening.  X  200.  (Green.) 

Fig.  46 


Fatty  degeneration  of  the  heart,  from  a  case  of  pernicious  anemia.  The  protoplasm  is 
replaced  by  globules  of  various  sizes  stained  black  by  osmic  acid.  The  outlines  of  the  fibers 
are  irregular,  owing  to  inequality  in  their  distention.      X  400.     (Green.) 

phorus  and  then  fed  with  fat  foreign  to  the  animals;  the  foreign 
fat  was  found  in  the  degenerated  cells. 

Causes. — Depression  of  vitality  is  always  the  proximate  cause,  and 
as  primary  causes  producing  this  depression  may  be  mentioned: 

Tissue  starvation  from  any  cause,  as  from  an  altered  food  supply. 
The  lack  of  oxygen  in  acute  hemorrhage  (suboxidation).     The  intro- 


DEFICIENCY  OF  NUTRITIOX.     HYPONUTRITIOX  75 

cluction  into  the  blood  of  toxic  substances,  such  as  mineral  poisons, 
e.  g.,  arsenic,  mercury,  or  phosphorus;  chemical  compounds,  as  carbon 
monoxide;  leukomaines,  as  in  diabetes  and  chronic  anemia;  toxins,  as 
in  fever  of  bacterial  origin  or  from  a  focus  of  infection.  Locally, 
interference  with  the  circulation,  if  not  sufficiently  overwhelming  to 
produce  death,  may  cause  fatty  degeneration  of  cells  by  interfering 
with  the  food  supply  as  in  venous  hyperemia,  aseptic  infarcts,  and 
simple  inflammation.  The  products  of  infection  can  produce  fatty 
degeneration  in  the  cells  of  the  inflamed  area.  (See  Pathology  of 
Inflammation.) 

Fig.  47 


•'C'/  ,  ..         '  :^/ 


x" 


Cloudy  swelling  of  kidney  epithelium:  a,  normal  epithelium:  b,  epithelium  beginning  to  be 
cloiuly;  c,  advanced  degeneratiiDn;  d,  cast-off  degenerated  epithelial  cells.  From  a  preparation 
which  had  been  treated  with  ammonium  chromate.      X  600.     (Ziegler.) 

In  areas  which  have  undergone  fatty  degeneration  a  cheesy 
substance  may  be  formed  out  of  the  degenerated  elements  exist- 
ing in  the  part.  The  fluid  is  gradually  absorbed  and  a  mass  com- 
posed of  atrophied  cells,  fatty  debris,  and  cholesterin  crystals  is  left. 
This  process  is  known  as  caseation.  Encap.sulation  of  the  caseous 
mass  by  fibrous  tissue  may  take  place,  or  its  liquefaction  or  its  calcifica- 
tion may  occur.  Fatty  degeneration  may  occur  in  many  tissues,  and 
the  danger  is  proportionate  to  the  importance  of  the  tissue  involved. 

Cloudy  Swelling  (Parenchymatous  or  Granular  Degeneration). — 
Cloudy  swelling  is  a  change  occurring  in  the  parenchyma   (essential 


76  DISTURBANCES  OF  NUTR.ITIOX 

cells)  of  a  part  as  the  result  of  the  presence  of  toxic  substances  in  the 
blood,  or  even  as  the  result  of  aseptic  disturbance  of  nutrition,  such  as 
a  severe  burn.  The  same  causes  which  produce  fatty  degeneration 
may  produce  it. 

Pathology. — The  cell  absorbs  fluid,  swells,  its  contents  become  gran- 
ular, and  the  histological  structure  is  lost.  In  the  early  stages  the 
change  is  albuminous;  no  fat  is  demonstrable;  later,  however,  it 
appears,  so  that  the  change  is  regarded  as  a  first  stage  in  the  produc- 
tion of  fatty  degeneration,  by  which  process  many  of  the  cells  are  lost, 
though  the  organ  may  recover  if  the  patient  withstands  the  original 
disease  (Fig.  47). 

Glycogenic  Infiltration. — Normally,  glycogen  is  found  in  some  other 
tissues  than  those  of  the  liver,  notably  in  muscle.  If  it  appear  in 
tissue  not  normally  containing  it,  or  in  excess  in  those  in  which  it 
is  normal,  a  glycogenic  degeneration  or  infiltration  exists.  It  may  be 
produced  by  any  influence  which  alters  the  behavior  of  cells,  espe- 
cially those  having  secreting  activity  toward  the  carbohydrate  food 
element  (glucose)  as  in  diabetes,  and,  while  mostly  within  the 
cells,  may  exist  in  the  intracellular  tissue  (Stengel).  It  is  stained 
brown  by  iodine  and  converted  by  ptyalin  or  amylopsin  into  sugar, 
the  color  reaction  then  not  occurring. 

It  does  not  seem  to  be  clearly  shown  as  a  direct  infiltration  of 
glycogen,  but  rather  as  an  appearance  of  glycogen  in  the  cells,  which 
may  readily  be  glucose  changed  to  glycogen  within  the  cells.  It 
has  not  been  satisfactorily  shown  to  be  a  degeneration  from  proteid 
constituents  (Stengel). 

Cook^  calls  attention  to  the  fact  that  the  tissues  become  capable  of 
diverted  action,  and  that  the  glycogen  may,  even  experimentally,  be 
so  acted  upon  by  oxidizing  agents  as  to  be  converted  into  acid  deriva- 
tives, probably  lactic  acid,  paralactic  acid,  and  sarcolactic  acid,  and 
that  these  may  be  broken  up  by  the  zymotic  action  of  tissue  cells  or 
by  certain  bacteria.  The  degenerative  change  in  the  tissues  renders 
them  susceptible  to  bacterial  action,  as  in  case  of  the  gum  tissue. 

The  mucous  membrane  of  the  gums  has  })een  shown  by  the  same 
author  to  be  capable  of  this  degeneration  if  overstimulated  by  chem- 
ical agents  followed  by  the  use  of  a  stiff'  brush,  and  he  argues  that 
acid  derivatives  may  be  liberated  either  by  the  tissue  or  by  bacteria  in 
contact  with  them,  and  tluis  possibly  account  for  certain  phases  of 
tooth  destruction,  as  erosion.      He  emphasizes  the  fact  that  infiltra- 

'  Dental  Cosmos,  1907. 


DEFICIENCY  OF  NUTRITION.     HYPONUTRITION 


77 


tion  of  tissue,  with  abnormal  quantities  of  a  normal  constituent  of  the 
body,  is  more  likely  to  take  place  in  the  lymphoid  and  mucous  cells 
of  the  body  than  in  any  other  tissue  structure. 

Hyaline  Degeneration. — In  various  forms  of  arthritis,  in  arterio- 
sclerosis, (luring  infection,  in  septic  processes,  and  in  other  conditions 
a  retrogressive  process,  characterized  by  the  appearance  of  a  homo- 
geneous proteid  substance,  occurs.  It  is  closely  allied  to  amyloid, 
mucoid,  and  colloid  degeneration,  and  to  coagulation  necrosis.  The 
new  tissue  is  of  a  glistening,  waxy,  homogeneous  appearance,  and 
stains  with  great  affinity  with  acid  aniline  stains,  as  acid  fuchsin, 
taking  a  brilliant  red  color.  The  cells  of  the  j)art  may  show  fatty 
degeneration. 

Location. — Seats  of  interest  are  the  endothelium  of  bloodvessels 
which    is  proliferated,    making  the   wall    thickened,  the  lumen  nar- 

Fic.  48 


Hyaline  degeneration  of  small  vessels  in  the  cord.      X  350. 

rowed,  or  obliterated.  (See  Endarteritis  Obliterans.)  Upon  mucous 
membranes  it  causes  opaque  plates  or  pseudomembranes.  It 
occurs  in  interstitial  tissues  and  also  within  the  cells.  Its  jiroximate 
etiology  and  ])athology  are  obscure. 

The  hyaline  material  can  be  reconverted,  absorbed,  and  removed. 
It  does  not  injure  the  cells  to  an  extreme  degree.  It  may  be  converted 
into  other  albuminoid  degenerations,  may  undergo  caseation  and 
calcareous  infiltration  (Stengel).  It  has  i)cen  found  in  the  ej)itiielium 
of  the  mouth  by  Cook,  Init  without  established  significance. 

Mucoid  Degeneration. — In  this  form  of  degeneration  the  ])roteid 
protoplasm  oi  cells  is  transformed  into  mucin,  a  glycoproteid 
characterized  by  affinity  for  basic  aniline  stains,  as  methylene  blue. 
It  occurs  in  catarrhal  mucous  membranes,  connective  tissue,  tumors, 
etc.  Mucin  absorbs  water,  but  is  not  soluble  in  it  nor  dialyzablc. 
In  the  catarrhal  mucous  membranes    the   jroblet   cells  show  excess 


78 


DISTURBANCES  OF  NUTRITION 


in  number,  and  are  swollen  and  distended  with  mucin  (Stengel). 
The  cell  becomes  vacuolated  and  the  nucleus  granulates  and  stains 
with  a  basic  stain.  About  the  necks  of  teeth  the  mucus  becomes 
stringy  and  tenacious,  its  chemical  and  physical  character  being 
changed  and  chondroitin  present  (Cook).^ 

According  to  this  author  this  substance  combining  with  water  might 
give  rise  to  sulphuric  acid  in  contact  with  the  teeth.  C18H27NSO17 
+  H2O  =  HoSOi  +  C18H27NO14.  Mucic  acid  might  be  produced 
from  glycuronic  acid  found  in  mucin.  Cook  observed  mucoid  degen- 
eration of  epithelial  cells  and  submucous  structure  in  cases  in  which 
strong  astringents  were  used  on  the  mucous  membrane;  the  con- 
traction of  the  cells  caused  a  retention  of  mucin  leading  to  a 
chemical  change  in  the  mucin  itself.    (See  Erosion.) 

Fig  49 


Colloid  cancer,  showing  the  large  alveoli,  within  which  is  contained  the  gelatinous 
colloid  material.      X  300.     (Rindfleisch.) 

Colloid  Degeneration. — This  consists  of  the  abnormal  appearance 
of  a  non-dialyzable  substance  like  mucin,  but  differing  from  it  in 
preference  for  acid  stains,  by  not  being  precipitated  by  acetic  acid 
and  alcohol,  by  lack  of  absorption  of  water,  also  by  causing  a  more 
profound  disturbance  of  cells  in  which  this  is  found  and  in  which 
it  remains  much  longer.  Salts,  as  calcium  oxalate,  are  apt  to  be 
precipitated  in  it,  and  may  be  again  dissociated.  The  etiology  is 
obscure,  but  probably  analogous  to  that  of  mucoid  degeneration. 

Dropsical  Inlfiltration. — ^This  is  an  infiltration  of  an  excess  of 
plasma  into  cells.  It  is  a  part  of  cloudy  swelling,  or  may  occur  as 
large  droplets  of  plasma  enlarging  the  cell  compressing  the  nucleus 


1  Dental  Cosmos,  1907 


DEFICIEXCY  OF  NUTRITION.     HYPONUTRITION  79 

and  protoplasm,  and  may  even  cause  the  cell  to  burst.  Fatty  degen- 
eration of  the  protoplasm  may  occur  as  a  sequence  to  dropsical 
infiltration.  The  process  occurs  in  general  dropsy,  in  burns,  in  skin 
lesions  connected  with  vesiculation,  and  in  inflammation  of  organs. 
Lardaceous  Degeneration. — This  type  of  degeneration  is  known 
as  amyloid,  albuminous,  or  waxy.  The  formation  of  the  material  from 
which  this  condition  derives  its  name  is  preceded  by  an  imknown  type 
of  degeneration  of  the  cells  of  the  part  affected.  The  degenerative 
processes  appear  to  be  the  result  of  long-continued  suppuration  due 
usually  to  tuberculous  disease.  In  the  connective  tissue  about  the 
degenerated  cells  (not  in  the  cells)  a  substance  akin  to  albumin  is 

Fig.  50 


^:«^-^,;gi^4^.ii'-7;; 


Calcareous  infiltration  of  renal   epithelia.     From  the  edge  of  an  old  infarct;  a  few 
tubules  still  to  be  recognized.      X  250.     (Schmaus  and  Ewing.) 

deposited,  which  causes  swelling  and  a  pseudohypertrophy  of  the 
organ  affected.  The  substance  gives  a  reaction  with  iodine  resem- 
bling that  of  starch;  hence  the  name  amyloid  {amylum,  starch).  It 
may  affect  any  organ  of  the  body.  It  usually  appears  first  in  the 
connective  tissue  lying  between  the  inner  and  midtlle  coats  of  small 
arteries.  The  swelling  caused  bv  tlic  infiltration  markedlv  lessens 
the  caliber  of  the  vessels  and  diminishes  the  nutritive  supply  of  the 
parts  supplied  by  the  artery,  which  may  lead  to  fatty  degeneration 
and  atrophy  of  the  insufficiently  nourished  parts. 

Calcareous  Infiltration. — In  tissues  which  have  undergone  pre- 
vious deoeneration,  calcium,  sodium,  or  mafrnesium  salts  mav  be 


80  DISTURBANCES  OF  NUTRITION 

deposited  as  an  infiltration  from  the  blood  plasma.     The  parts  are 
thus  petrified.     The  cells  take  no  active  part  in  the  process.^ 

It  is  believed,  however,  that  the  deposit  of  salts  in  the  dying  tissue 
is  more  than  a  mere  precipitation,  and  that  calcification  results  from  a 
combination  of  the  salts  with  an  albuminous  base  and  with  fatty  acids, 
such  an  afiinity  being  favored  by  the  degenerative  changes.  Ordina- 
rily the  carbonate  and  phosphate  of  calcium  are  the  infiltrating  salts, 
but  in  gout,  uric  acid  salts  are  deposited,  owing  to  an  excess  of  uric 
acid  in  the  form  of  biurates  and  quadurates  in  the  body  fluids. 
A  sluggish  circulation  in  the  part  favors  the  deposition  of  the  salts. 
The  calcification  may  occur  in  both  the  cells  and  in  the  inter- 
cellular substance.^  (See  Calcific  Degeneration  of  the  Pulp.)  In  the 
early  stages  the  salts  are  found  as  fine  granules  in  the  intercellular 
substance. 

"The  white,  fibrous  tissue  is  the  form  of  connective  tissue  usually 
affected,  but  concretions  may  occur  in  the  connective  tissue  surround- 
ing the  bloodvessels."^ 

As  a  secondary  process  after  degeneration,  calcification  of  the  middle 
coats  of  the  arteries  may  occur  rendering  them  inelastic.  This  renders 
them  incapable  of  regulating  the  blood  supply  to  parts,  and  these  suffer 
more  or  less  nutritive  disturbance,  and,  in  some  cases,  actual  death 
of  the  part  (gangrene).  Calculi  are  found  in  tumors  at  times.  Many 
forms  of  free  calculi  are  formed  in  the  body.  These  occur  most  fre- 
quently in  ducts  or  cavities  lined  with  epithelium — e.  g.,  the  salivary 
ducts  and  the  bladder. 

"All  free  concretions  have  an  organic  basis  or  nucleus,"  with  which 
are  combined  the  calcium  salts,  oxalates,  cholesterin,  etc.,  making  up 
the  inorganic  or  crystallizable  part  of  the  combination.  The  organic 
part  may  consist  of  inspissated  feces,  as  in  enteroliths,  mucus,  or 
mucin,  as  in  the  calculi  upon  the  teeth;  epithelial  scales,  mucus,  etc., 
in  the  urinary  passages.*  The  fine  crystals  or  granules  are  probably 
soluble  in  some  cases.  The  larger  calculi  are  probably  permanent 
and  cause  degeneration  of  adjacent  tissue. 

Calcareous  infiltration  is  clearly  to  be  distinguished  from  the  normal 
calcification  of  the  hard  tissues,  bone,  enamel,  dentine,  and  cementum. 
These  are  composed  of  calcoglobulin,  in  which  calcium  and  mag- 
nesium salts  are  combined  under  the  superintendence  of  certain 
living  cells  with  albuminous  bases  derived  probably  from  their  own 
suh>stance. 

'  Green,  Pathology  and  Morbid  Anatomy.  -  Zieglei,  Geneial  Pathology. 

«  Ibid.  4  Ibid. 


NECROSIS  81 

Pigmentary  Infiltration. — Pigmentary  infiltration  is  the  infiltration 
of  coloring  matter  into  the  tissues.     There  are  four  varieties: 

1.  Extrinsic,  derived  from  outside  the  body,  c.  (/.,  coal  dust  in  lung 
tissue  or  general  staining  from  silver  salts  taken  up  in  the  intestines. 

2.  Hematogenous,  derived  from  hemoglobin  or  its  derivatives. 
They  are : 

(a)  Hemoglobin,  dark  red. 

{h)  Hemin,  red(hsh  brown  f)r  bluish  black. 

(c)  Methemoglobin,  l)rownisli  red. 

(d)  Hematin,  (hirk  brown  or  bluish  black. 

(e)  Hematoidin,  orange  or  reddish  brown. 
(/)  Hemosiderin,  yellowish  or  brownish. 

These  are  decomposition  products  of  hemoglobin.  Hemoglobin 
and  hemositlerin  contain  iron. 

3.  Hepatogenous,  or  biliary. 

4.  Metabolic,  resulting  from  cellular  activity  within  the  body,  and 
termed  melanin. 

The  hematogenous  pigments  are  of  chief  interest,  inasmuch  as  they 
occur  in  the  staining  of  teeth  by  devitalized  pul[)s  and  sometimes  by 
living  pulps  in  a  state  of  venous  hyperemia.  In  these  (Hscolorations 
there  is  analogy  to  the  colors  manifested  in  an  old  bruise,  which 
undergo  various  color  changes  as  the  chemical  character  of  the  pig- 
ment is  altered.     (See  Moist  Gangrene  of  the  pulp.) 


NECROSIS. 

Necrosis  (from  uelcros,  dead)  signifies,  in  its  broadest  sense,  death 
of  tissue.  It  is  due  to  profound  disturbance  of  its  nutritional  func- 
tion or  to  direct  injury  to  its  elements. 

Necrosis  j)roper  {per  se)  signifies  death  of  tissue  in  mass  from  any 
cause. 

Necrobiosis  means  the  deatli  of  cells  tlu'ough  the  process  of 
atrophy  or  degeneration,  wliich  are  successive  changes  leading  to 
death. 

Necrosis  of  bone  signifies  the  circumvallation  and  deatli  of  bone 
through  tiie  process  of  inflammation,  which  causes  thrombosis  of  its 
vessels  and  cessation  of  its  luitrition.  The  dead  jnirt,  wlien  separated, 
is  called  a  sequestrum.  The  solution  of  contituiity  is  effected  l)y 
leukocytes  massed  about  the  portion  in  which  nutrition  has  ceased. 
6 


82  DISTURBAXCES  OF  NUTRITION 

Caries  of  bone  is  that  form  of  bone  death  in  which  the  bone  is 
honey-combed  and  molecularly  broken  down  rather  than  sequestrated. 
(See  Osteoporosis.) 

Gangrene  is  a  term  used  to  signify  death,  en  masse,  of  a  part,  the  soft 
parts  being  included.  The  dead  part  undergoes  drying  (dry  gangrene) 
or  putrefactive  softening  (moist  gangrene).     (See  Gangrene.) 

Etiology. — The  causes  of  necrosis  are  as  follows : 

1.  Circulatory  obstructions,  as  (a)  stoppage  of  an  artery  supplying  a 
part,  the  nutritive  supply  being  cut  off  by  any  cause.  (6)  Venous 
hyperemia  of  a  part,  the  vein  being  unable  to  carry  off  the  blood 
charged  with  cellular  waste,  which  accumulates  about  the  cells,  in- 
toxicates them,  and  presents  access  of  fresh  blood  (food  supply),  (c) 
Occlusion  of  the  capillaries  by  any  cause  has  a  similar  effect.  Inflam- 
mation may  be  placed  in  this  general  class  of  causes. 

2.  Trophic  Disturbances. — The  nerves  controlling  the  metabolism 
of  a  part  being  diseased,  the  part  undergoes  degeneration  and  slight 
causes  produce  necrosis — e.  g.,  necrosis  of  eyeball  when  excision  of 
the  Gasserian  ganglion  has  been  practised. 

3.  Direct  destrux^tion  of  the  vital  activities  of  cells  by  any  physical  or 
mechanical  agents,  or  chemical  substances,  including  among  the  latter 
the  poisonous  substances  produced  through  the  action  of  bacteria. 

Injuries,  blows,  the  tension  of  exudate,  pressure,  excessive  heat  or 
cold,  the  passage  of  powerful  electric  currents  and  the  x-rays  are  all 
influences  which  directly  injure  or  permanently  destroy  vital  activities 
of  cells.  The  application  of  chemical  agents  which  so  act  upon  cell 
substance  as  to  change  its  character  produces  necrosis. 

While  this  is  particularly  true  of  such  substances  as  powerful  acids 
and  alkalies,  or  alkaloids,  which  immediately  destroy  cell  integrity,  it 
is  also  true  of  milder  agents  acting  for  longer  periods.  Certain  poisons, 
particularly  those  of  bacterial  origin,  paralyze  the  vital  activities  of 
cells,  and  necrosis  results. 

The  occurrence  or  non-occurrence  of  or  the  liability  to  necrosis  will 
largely  depend  upon  the  degree  of  vital  energy  of  cells  prior  to  the 
action  of  the  active  causes  of  necrosis.  Parts  debilitated  from  any 
cause  are  more  liable  to  necrosis  than  those  which  have  suffered  no  . 
debility.  A  part  chronically  ill-nourished,  subjected  to  the  causes 
prodiicing  degenerations,  is  liable  to  suffer  necrotic  changes,  for  the 
several  degenerations  and  atrophy  are  but  successive  stages  leading 
to  necrosis. 

A  necrosed  part  acts  as  an  irritant  to  the  tissues  about  it,  inaug- 


GANGRENE  83 

urating  an  inHainnuitory  reaction  which  marks  oli'  tlic  dead  from 
the  hving  parts.  Tiie  dead  part  is  seqnestered,  and  hence  is  called  a 
sequestrum  or,  in  case  of  soft  parts,  a  "slough,"  or  sphacelus. 

Necrosis  may  be  of  several  types*,  of  which  the  following  are  the 
chief  forms: 

Coagulation  Necrosis. — When  a  dying  tissue  contains  coagulable 
material  and  the  necessary  ferments,  the  parts  undergo  coagulation. 
(See  Coagulation.)  The  cells  and  parts  about  become  solidified,  the 
cells  lose  their  nuclei  and  do  not  stain  as  usual,  the  part  appears 
glazed,  pale,  and  waxy.  It  occurs  in  suppuration,  and  is  due  to  the 
coagulating  ferments  of  pyogenic  cocci.      (See  Bacterial  Ferments.) 

The  thrombosis  of  the  vessels  about  an  area  of  infective  inflamma- 
tion is  probably  due  to  the  same  ferments. 

Fat  Necrosis. — This  is  a  peculiar  form  of  fat  death  in  which  the  fat 
is  split  into  glycerin  and  fatty  acid  by  lipase  (a  ferment).  The  fatty 
acid  remains  and  combines  with  inorganic  salts. 

Liquefaction  Necrosis. — This  is  the  death  of  tissue  with  liquefaction 
of  the  proteid  material  in  the  area,  which  is  usually  rich  in  exudates. 
The  process  is  probably  due  to  enzymes  capable  of  liquefying  the 
tissue. 

GANGRENE. 

When  death,  en  masse,  of  a  ])art  occurs  as  the  result  of  an  interference 
with  its  nutritive  supply,  the  process  is  termed  gangrene. 

Causes. — It  may  occur  as  the  result  of  an  inflammation  produced 
by  a  particular  bacterium,  as  in  noma  or  malignant  edema;  from 
arterial  obstruction,  as  arterial  thrombosis;  or  capillary  obstruction,  as 
in  freezing  or  venous  obstruction,  may  produce  it.  (See  Venous 
Hyperemia  of  the  Pulp.)  Ergot  may  produce  it  through  contraction 
of  the  bloodvessels. 

Dry  Gangrene. — In  parts  which  ordinarily  contain  but  little  fluid 
the  obstruction  of  the  artery  may  be  associated  with  but  little  obstruc- 
tion of  the  veins  and  lymphatics.  Under  such  circumstances  the  dead 
part  is  drained  of  the  little  fluid  it  contains,  and  a  fresh  access  of  fluid 
is  prevented.  Plxposure  to  the  air  aids  a  further  loss  of  moisture  by 
evaporation.  The  conditions  are  not  favorable  to  the  development  of 
microorganisms,  and  the  part  changes  from  a  ])ale  aj)}>earance  to  a 
dark,  shrunken  one.  The  process  of  gradual  drying  is  also  called 
mummification.  (See  Dry  Gangrene  of  the  Pulj).)  It  is  usuallv 
circumscribed. 


84  DISTURBAXCES  OF  NUTRITION 

Moist  Gangrene. — Under  opposite  conditions — i.  e.,  a  venous 
obstruction  with  a  weak  arterial  supply — there  is  much  venous 
engorgement  and  extravasation  of  blood  into  the  tissues,  which  are 
stained  red  by  the  hemoglobin  from  disintegrated  red  corpuscles. 
Abundant  effusions  also  cause  the  part  to  be  swollen.  Death  of  tissue 
occurs  from  interference  with  nutrition;  when  bacteria  are  the  direct 
cause  the  part  is  inflamed  and  edematous.  The  moisture  present 
favors  the  development  of  bacteria,  and  they  enter  the  tissue  through 
the  skin.  Putrefaction  with  the  evolution  of  malodorous  gases,  such 
as  hydrogen  sulphide  (HjS),  hydrogen  phosphide  (HPg),  and  ammo- 
nium sulphide,  (NH^)2S,  causes  the  part  to  have  an  offensive  odor. 

If  the  gangrene  be  due  to  infective  inflammation,  or  the  surrounding 
tissue  be  debilitated  from  any  cause,  the  area  of  gangrene  may  spread 

Fig.  51 


6 

Or 

Senile  gangrene  of  the  great  toe,  from  a  case  of  arterial  thrombosis.  The  toe  is  shrunken 
and  its  epidermis  is  being  exfoliated.  At  the  line  of  demarcation  the  skin  has  retracted  (a) 
and  the  deeper  parts  are  .separating  (6).     (Green.) 

— i.  e.,  invade  the  living  tissue  (spreading  gangrene).  This  is  probably 
fhie  to  the  presence  of  bacteria,  which  irritate  and  progressively  destroy 
the  surrounding  tissue.  The  poisons  produced,  if  absorbed,  may  cause 
death.  If  the  adjacent  tissue  be  healthy  and  resistant,  a  line  of 
demarcation  is  established,  consisting  of  leukocytes,  which  dissolve 
all  fibers  or  firm  connections  between  the  dead  and  living  parts. 
Suppuration  occurs  at  the  line,  and  the  dead  portion  is  separated 
as  a  sphacelus  or  slough.  Occurring  in  bone,  this  is  called  a  seques- 
trum. Occasionally  the  part  being  internal  is  encysted  and  the 
contents  may  be  absorbed  and  the  sac  calcified.'    An  ulcerated  surface 

'  Stengel,  A  Text- book  of  Pathology. 


GENERAL  MALXUTRITIOX  85 

is  left.  The  latter  form  is  circuni.scril)e(l  gangrene.  If  gangrene  he 
deep-seated  and  septic,  suppuration  occurs,  which  establishes  one 
or  more  fistulse  upon  the  surface  of  the  body  or  in  one  of  its  cavities. 
(See  Moist  Gangrene  of  the  Pulp.)  A  sequestrum  may  be  cast  out 
through  one  of  these.  In  the  aged  atheromatous  or  calcareous 
changes  in  the  arteries  produce  a  slow  circulation  in  the  extremities. 
A  slight  injury  to  a  vessel  wall  may  induce  extensive  thrombosis 
(which  see).  The  result  is  gangrene  of  a  part  or  all  of  an  extremity, 
known  as  senile  gangrene  (Fig.  51). 


GENERAL    MALNUTRITION. 

By  the  tei'm  malnutrition  is  meant  a  more  or  less  general  dis- 
turbance of  the  metabolic  processes  of  the  cells  of  the  body,  which  may 
sim])ly  lower  the  body  resistance  or  health  standard,  or  may  be  of 
such  profound  character  as  to  incapacitate  an  indivichial  for  ordinary 
functions. 

If  imperfect  digestion,  assimilation,  or  elaboration  of  food  materials 
or  its  circulation,  or  an  imperfect  relation  between  the  amount  of 
oxygen  and  food  material  at  the  cell  exist,  or  if  a  great  excess  of  food 
material  be  assimilated  which  cells  cannot  appropriate,  and  the  excess 
acts  as  material  to  be  gotten  rid  of,  or  if  the  food  taken  be  of  an  irritat- 
ing nature,  or  if  such  material  as  retained  body  waste  products,  toxins 
derived  from  foci  of  infection,  or  from  alimentary  canal,  or  drugs 
absorbed  are  presented  to  the  cells  in  excess,  or  if  the  drain  upon  the 
body  cells  reduce  the  amount  of  cell  protoplasm,  and  the  replacement 
of  the  cell  constituents  is  not  rapid  enough  to  restore  the  protoj)lasm 
wasted  in  energy,  it  is  plain  that  a  general  disturbance  of  body  cells 
may  result,  and  the  altered  metal)()lism  in  turn  furnishes  its  share  of 
irritating,  unfinished  catabolic  j)r()ducts  to  further  increase  the 
general  disturl)ance  through  the  ])r()(hietion  of  a  jxithological  (•()n(H(i()n 
of  the  blood  (a  humoral  condition,  Michaels).  The  gradual  action  of 
one  or  other  of  these  classes  of  causes,  acting  either  by  starving  the 
cells  or  by  irritating  them  (auto-intoxication),  produces  a  condition 
with  tendency  to  diseases  of  certain  type,  and  the  tendency  is  called 
diathesis  (acquired). 

According  to  Michaels,'  following  (lautrelet.  the  abnormal  \it;d 
processes  tend  in  mankind  to  ])ath()l()gical  conditions,  wliicli  we  may 

*  SlaKiseiiiioloK.V,  I'looeediiiKs   Tliinl  International   Dental  C"ivn(iie>s,   1900. 


86  DISTURBAXCES  OF  XUTRITIOX 

classify  under  two  humoral  conditions  (or  diatheses),  viz.,  hypo-acidity 
and  hyperacidity.  The  first  state  ("lymphatism")  is  the  expression 
of  a  vital  overactivity  and  has,  as  consequences,  the  contagious 
diatheses  (scrofula,  tuberculosis,  syphilis).  The  oxidations  are 
overactive,  and  the  hydrations  are  superior  to  the  normal,  hence 
there  is  a  decrease  in  organic  acidity  and  an  increase  of  saline  chlorides 
excreted  by  the  economy.  Hypo-acidity  favors  chemical  changes 
in  the  tissues  (Ducleaux).  In  the  hypo-acid  diathesis  all  the  oxida- 
tions are  exaggerated,  and  are  above  the  normal. 

"In  the  h}"peracid  diathesis  (arthritism), gout, rheumatism,  sclerosis, 
oxidation  is  insufficient;  there  is  incomplete  oxidation  with  a  con- 
sequent increase  of  organic  acidity  or  hyperacidity,  and  a  peculiar 
state  of  the  organism  characterized  in  a  general  way  by  a  slowness 
in  the  biochemical  changes.  The  reaction  of  the  blood  with  the 
ordinary  reagents  (litmus,  for  example)  is  normally  alkaline,  but 
if  we  study  the  distribution  of  the  acids  and  bases  of  the  blood  plasma 
we  see  that  the  reaction  is  really  acid  (Gautrelet,  Drouin,  and  Hugeou- 
nenq),  and  thus  acidity  is  increased  and  the  blood  may  become 
decidedly  acid  by  the  accumulation  of  acid-waste  products  which 
are  not  eliminated,  the  secretions  and  excretions  becoming  then 
of  acid  reaction.  It  is  on  this  account  that  a  certain  number  of 
chronic  diseases  have  constant  characteristics  in  regard  to  semi- 
ology; increase  of  the  normal  acidity  of  the  urine,  as  well  as  the  increase 
in  the  normal  acidity  of  the  saliva."  Following  Gautrelet,  he  gives 
four  effects  of  the  exaggerated  and  retrograde  processes  that  diath- 
esis produces:  (1)  A  chemical  modification  of  the  plasma;  (2) 
modifications  affecting  the  chemistry  of  secretions  and  excretions 
(as  detailed  above) ;  (3)  histological  modifications  in  the  tissues;  (4) 
modifications  due  to  the  creation  of  a  special  field  for  microorganisms. 
It  will  be  seen  that  the  above  effect  begins  with  a  change  in  the 
l)lood  or  its  contents,  which  successively  acts  upon  glandular  and  other 
cell  physiology  and  later  alters  their  histology,  and  in  total  may 
bring  about  a  predisposition  to  bacterial  invasion  through  the  loss 
of  vital  potential  or  resistance.  The  hyperacid  diathesis  may  be 
inherited  or  acquired  by  individuals  who  take  a  liberal  supply  of 
food  requiring  oxidation  and  take  insufficient  exercise  in  the  open 
air,  while  in  the  hypo-acid  the  oxidation  is  superior  to  normal. 

These  diatheses  arc  the  forerunners  of  many  of  the  diseases  of 
rnulmitrition,  and  evidence  of  approaching  disease  may  be  obtained 
from  both   saliva  and   urine  by  analysis  of  their  contents  through 


GENERAL  MALXUTRITIOX  87 

physical,  chemical,  and  raicropolariscopic  examination  of  either  or 
both  fluids.  The  contents  of  each  fluid  being  taken  out  of  the 
blood  through  glandular  activity  represent  fairly  the  faulty  elements. 
The  presence  of  altered  physical  characteristics  when  fresh  or  upon 
standing,  of  unusual  chemical  substances  determinable  either  bv  the 
aid  of  reagents  or  microscopic  or  micropolariscopic  examination, 
leads  to  the  inference  that  unusual  chemical  changes  have  occurred 
in  the  cells,  or  that  the  waste  products  found  represent  an  undue  waste 
of  tissue,  or  that  cell  waste  has  been  altered  after  leaving  cells  or 
not  sufficiently  changed  into  the  normal  waste  products. 

In  the  accentuated  disease  condition  one  or  more  organs,  as  the 
liver  and  kidney,  may  be  diseased,  and  it  may  be  a  nice  point  to 
determine  whether  the  disease  begins  with  the  liver  and  proceeds  to 
the  diathesis,  or  with  the  diathetic  condition  or  its  cause  and  proceeds 
to  disturb  the  liver.  At  the  same  time  the  same  course  might  act 
upon  both;  for  example,  overfeeding  with  food  requiring  oxidati(m, 
and  this  not  supplied  by  exercise,  could  induce  a  disturbance  of  the 
function  of  liver  cells  quite  as  readily  as  of  any  other  l^ody  cells. 

According  to  Kirk,'  the  disproportion  between  pabulum  and  oxygen 
resulting  in  hyperacidosis  produces  a  greater  ratio  of  carbon  dioxide 
to  oxygen  in  the  blood  than  is  normal.  Temporarily  this  would  be 
corrected  by  the  action  of  the  renal  epithelium  in  which  a  reaction 
occurs  between  the  carbonic  acid  of  the  blood  and  the  basic  phosphates, 
as  follows:  HNa2Po,  +  H2C03  =  H^NaPo,  +HXaCo3.  The  sodium 
bicarbonate  formed  is  returned  to  the  blood,  maintaining  its  alkalinity, 
and  the  acid  sodium  phosphate  is  eliminated  as  the  normal  acid  salt 
of  the  urine.     In  the  same  way  acid  calciimi  phosphate  is  formed. 

When  the  disproportion  between  pabulum  and  oxygen  are  con- 
tinued, the  suboxidation  becomes  chronic,  the  kidney  is  no  longer 
sufficient  to  maintain  alkalescence  of  the  blood  by  eliminating 
the  excess  of  acidity  as  acid  phosphate,  the  carbonic  acid  seeks 
other  channels  of  elimination,  and  the  epithelium  of  the  buccal 
glands  and  sweat  glands  may  take  up  the  action  normal  to  the  kidney 
and  excrete  acid  sodium  phosphate  and  acid  calcium  phosphate, 
producing  in  the  case  of  the  buccal  glands  a  certain  class  of  erosion  of 
the  teeth,  and  in  the  case  of  the  sweat  glands  frequently  giving  rise 
to  eczematous  eruptions.  Dental  caries  is  not  ordinarily  induced  in 
this  stage,  but  if  Ix^gun  the  carious  matter  is  ciiang(>d  to  a  (hirk  brown 
color,  crumbly,  semiiiard  texture,  and  the  furtluM-  proccvss  is  one  of 
decalcification  rather  than  a  true  carious  process. 

'  Dental  Review.  1903. 


8g  DISTURBAXCES  OF  XUTRITIOX 

"The  continued  suboxidation  and  hyperacidosis  by  carbonic  acid 
thus  leads  to  the  great  loss  of  basic  phosphates  as  acid  phosphates, 
which  are  more  readily  soluble  and  osmosed  through  kidney  epithelium 
than  basic  phosphates,  and  for  that  reason  are  rapidly  eliminated, 
thus  establishing  a  phosphaturia,  with  consequent  phosphatic  star- 
vation and  ill  health,  as  shown  by  neurasthenia,  with  its  irritability, 
despondency,  migraine,  cerebral  hyperemia,  or  hysterical  phenomena. 
A  point  of  depletion  is  reached  and  they  are  found  only  in  minute 
quantity  in  the  urine  and  saliva.  At  about  this  time  lactates  of 
sodium,  calcium,  and  magnesium,  in  the  order  named,  appear  in  the 
saliva,  then  double  lactates  of  sodium  and  calcium,  then  lactophos- 
phates  of  calcium  and  magnesium,  then  oxalate  of  sodium  or  double 
oxalate  of  sodium  and  calcium,  while  oxalate  of  magnesium  may 
appear  in  the  urine.  With  the  appearance  of  the  lactophosphate  a 
general  rather  than  a  localized  erosion  appears.  (See  Erosion.)  The 
nervous  irritability  is  markedly  increased,  and  a  rapid  loss  of  weight 
occurs.  Later,  acetone  and  diacetic  acid  appear  in  the  secretion  along 
with  creatin,  and  in  some  cases  cystin,  at  which  period  profound 
mental  torpor,  at  times  almost  amounting  to  coma,  is  not  infrequently 
manifested,  or  there  may  be  extreme  nervous  irritability  amounting 
almost  to  hysterical  mania. 

"Coincident  with  the  loss  of  the  phosphates,  nitrogen  with  carbon 
as  a  cyanogen  radial  (ammonium  cyanate),  which  probably  should 
have  gone  to  form  urea,  is  lost.  Evidences  of  imperfect  oxidation  of 
proteids  are  manifested  in  the  saliva  and  urine  by  the  presence  of 
lactate  of  ammonia  (a  forerunner  of  urea),  lactate  of  calcium,  creatin, 
acetone,  and  oxalates,  with  increase  of  urate  of  ammonia  and  amor- 
phous urates.  The  urine  often  contains  indican,  especially  in  cases 
complicated  with  disordered  liver  and  habitual  constipation.  The 
saliva  is  usually  constantly  acid,  due  to  the  presence  of  acid  phos- 
phates, and  the  dental  lesions  are  ordinarily  erosion ,  or,  where  the  acidity 
is  absent,  pyorrheal  invasion  of  the  peridental  membranes.  Many  of 
these  cases  develop  epithelioma  or  leukoplakia  buccalis,  or  both 
together,  and  in  view  of  the  fact  that  there  is  constant  irritation  of 
epithelium  by  the  exudates,  they  may  have  an  etiological  relation." 
(Free  (flotation.  Editor.) 

Tlie  diet  indicated  by  Kirk  for  these  cases  would  apply  to  those 
diseases  and  cases  of  pyorrlica  in  which  the  predis})osition  is  (hie  to 
this  diathetic  fault,  and  consists  in  reducing  the  necessity  for  oxygen 
by  largely  eliminating  the  carbohydrate  portion  of  the  diet.    Succulent 


OEXKRAL  ^tAL^'UTRITI(>^^  g9 

vegetables,  gluten  bread,  milk,  albumin,  and  a  motlerate  ration 
of  proteids  in  the  shape  of  fish,  oysters,  game,  light  meat  of  fowls, 
are  allowed.  Small  doses  of  phosphorus,  or  of  arsenic  iodide,  and 
glycerophosphates  of  lime  and  soda  are  continuously  administered. 
The  exercise  and  rest  are  adjusted,  and  attention  is  given  to  general 
hygiene. 

"Michaels  has  found  tlie  saliva  of  but  few  individuals  to  be  in  a 
perfectly  normal  condition  and  the  teeth  perfect,  while  most  of  them  are 
out  of  equilibrium  and  the  teeth  are  affected  either  by  caries  or  erosion 
or  pyorrhea  alveolaris.  He  states  that  lesions  of  the  liver  and  kidneys 
cause  the  appearance  of  acid  waste,  also  that  the  organism  constantly 
produces  acids,  such  as  uric,  oxalic,  lactic,  volatile  fatty  acid,  etc., 
which,  under  normal  conditions  are  also  destroyed,  l)ut  that  abnormal 
conditions  arise  which  retard  the  oxidations  of  these  organic  acids, 
which  must  then  accumulate  in  the  organism  among  the  waste  products 
arising  from  incomplete  dissimilation ;  many  have  acid  properties. 

"The  serum  of  venous  blood,  while  weakly  alkaline,  has  a  real  acidity 
(acid  elements)  stronger  than  that  of  arterial  blood.  Fever  is 
accompanied  by  an  acidity  of  the  blood,  as  is  diabetes  ((9-oxy butyric 
acid),  rheumatism,  arthritism  (gout).  The  alkalinity  is  reduced  (real 
acidity  increased)  in  anemia,  leukemia,  and  all  cachexias. 

"He  regards  the  liver  as  determining  the  majority  of  nutritive 
changes,  and  that  it  suffers  from  the  influence  of  all  sorts  of  toxins, 
whether  the  result  of  microbic  activity  or  due  to  an  excess  of  alkaloids 
(leukomaines).  The  cells  of  diathetic  inthviduals  constantly  elaborate 
products,  some  of  which  are  positively  poisonous  to  the  hejwtic  gland. 
The  acid  salts  and  biliary  pigments  are  toxic.  Their  absorption  is 
deleterious  and  the  inactivity  of  the  hepatic  cells  creates  a  danger  to 
the  organism.  The  danger  arises  from  the  fact  that  the  liver  has  to 
eliminate  from  the  circulation  all  kinds  of  debris.  If  the  neutraliza- 
tion of  the  products  of  fermentation  is  incomplete;  if  the  harmful 
ammoniacal  compounds  have  not  been  changed  into  urea;  if  the  liver 
does  not  have  a  reserve  of  glycogen,  or  if  its  generators,  which  are 
supposed  to  play  a  role  in  the  metamorphosis  of  alkaloids,  if  through 
its  inactivity  there  is  a  retention  of  waste  products,  the  secretions  are 
necessarily  contaminated  with  the  morbid  principles;  the  toxic  prod- 
ucts present  in  the  blood  poisons  the  organism  and  constitutes  the 
different  diatheses  (auto-intoxication)." 

This  conception  includes  the  views  of  physiologists  that  the  liver  is 
both  a  secreting,  excreting,  and  food  elaborating  organ.    He  argues  tliat 


90  DISTURBANCES  OF  NUTRITION 

if  the  bacteria]  fermentations,  by  their  presence  or  by  the  presence  of 
their  toxins,  are  capable  of  modifying  the  enzymic  secretions,  they  neces- 
sarily influence  the  action  of  the  physiological  fermentations.  It  follows 
from  this  that  these  toxic  principles  saturate,  in  a  given  period  of 
time,  the  organic  secretions  and  produce  a  cacochymic  state  (morbid 
state  of  the  body  fluids). 

]Michaels  has  found  in  the  saliva  of  hypo-acid  individuals  glycogen, 
albumin,  perhaps  inosite,  mucin,  basic  chlorides  with  ammonia  in 
greater  quantities  than  normally,  sulphocyanides  and  biliary  acid  in 
less  proportion  than  normally,  and  concludes  that  it  is  an  ideal  medium 
for  the  development  of  microbic  contagion.  He  has  found  glycogen 
in  the  saliva  of  adolescents  generally,  and  susceptible  of  reduction  and 
fermentation  under  the  influence  of  ptyalin  in  the  presence  of  earthy 
salts,  a  fact  emphasized  by  Kirk  with  a  view  to  its  establishment 
as  a  prominent  factor  in  susceptibility  to  caries  (which  see).  In 
the  saliva  of  hyperacids  he  found  sulphocyanides  and  mineral  and 
organic  acids,  acid  phosphates  of  sodium  and  potassium,  ammoni- 
acal  oxalates,  biliary  elements,  and  urobilin  in  greater  proportions 
than  normally. 

The  increased  importance  of  the  consideration  of  metabolic  dis- 
eases in  their  relation  to  dental  diseases  by  the  dentist  warrants  the 
introduction  of  a  brief  summary. 

Inanition. — This  is  ultimately  tissue  starvation,  whether  due  to  any 
of  the  following  causes : 

1.  Want  of  proper  amount  of  food. 

2.  Gastric  diseases  interfering  with  digestion  by  altering  the  quality 
or  quantity  of  hydrochloric  acid  or  pepsin. 

3.  Disease  of  the  liver,  etc. 

4.  Abnormal  intestinal  digestion. 

5.  Occlusion  of  the  sorbefacients  by  retained  excrementitious  matter 
or  other  local  disease. 

Effects. — The  tissues  are  not  properly  supplied  with  food  to  main- 
tain themselves,  and  waste  exceeds  repair;  the  unimportant  parts  are 
first  consumed  and  make  good  the  deficiency.  The  surplus  food  mate- 
rials, first  the  fats,  are  first  consumed,  then  the  carbohydrates,  next 
the  nitrogenous  tissues,  first  muscles  and  glandular  organs,  and  lastly, 
the  osseous  and  nervous  tissues. 

This  is  general  atrophy  necessarily  accompanied  by  degeneration. 
There  is  loss  of  energy  and  temperature,  and  the  vital  organs  are  weak; 
death  occurs  from  exhaustion. 


GENERAL  MALXUTRITIOX  91 

Overfeeding. — ^Tlie  excessive  use  of  proteids  in  foot!  leads  to  a 
necessity  for  elimination  from  the  blood  of  the  excess  absorbed,  and  to 
intestinal  fermentation  of  the  unabsorbed  excess.  The  proteid  food 
maintains  the  proteid  P(niilibiiuin,  and  any  more  than  is  required  for 
this  is  in  excess. 

Energy  is  largely  supplied  by  the  carbohydrates  (eventually  glucose) 
and  the  fats.  An  excess  of  these  leads  to  the  storing  of  fat  to  a 
degree  normal  and  useful  as  a  reserve,  but  in  combination  with  a 
sedentary  mode  of  life,  pathological  fat  or  obesity,  in  which 
oxidation  is  reduced.  A  tendency  to  fat  production  exists  in  indi- 
viduals. 

Excessive  Tissue  Destruction. — The  tissues  may  be  excessively 
wasted  by  many  causes,  and  in  many  cases  the  food  supply  is  deficient 
as  well.    These  causes  are,  briefly: 

1.  Fevers. 

2.  Continuous  hemorrhage. 

3.  Long-continued  suppuration. 

4.  Tumors,  especially  carcinoma. 

5.  Chronic  infectious  diseases,  as  tulierculosis. 

The  increased  waste  is  due  either  to  increased  oxidation  of  the 
proteid  elements,  due  to  stimulation  of  nervous  centres  controlling 
catabolism,  or  to  the  ferment  contained  in  the  toxic  substances 
produced  and  entering  the  blood,  which  may  cause  cellular  waste  in 
the  effort  to  produce  antitoxins  (see  Ehrlich's  Side  Chain  Theory), 
while  at  the  same  time  normal  food  appropriation  is  interfered  with 
if  the  amount  of  food  supplied  is  not  indeed  lessened,  as  in  continuous 
hemorrhages. 

Intoxications. — These  may  be  divided  into  extrinsic  and  intrinsic 
intoxications.     The  ])rin('ipal  classes  are: 

1.  Intestinal  Intoxications. — In  intestinal  putrefaction,  particularly 
in  constipation,  the  aromatic  products,  acetone,  tyrosin,  indol,  skatol, 
phenol,  cresol,  and  paracresol,  may  be  absorbed  and  produce  a  form 
of  intoxication  of  tissue  cells  which  lowers  the  vital  potential  of  all 
cells  and  the  resistive  force  of  tissues  to  bacterial  infection.  In  in- 
testinal ])utrefa('ti()n  in  children  a  marked  readiness  of  the  muscular 
system  to  fatigue  has  been  noted,  also  in  cases  of  persons  who  have 
suffered  from  indicanuria  for  a  long  time,  showing  a  mark(>dly 
poisonous  effect  upon  muscle  and  probably  upon  other  tissue. 

The  absorption  of  indol  and  its  modification  in  the  liver  leads  to 
its  ap])earance  in  t\\v  wv'uw  as  indican,  or  indo\ylsulj>luit('  of  |)()tas- 


92  DISTURBAXCES  OF  NUTRITION 

siiim^  which,  therefore,  indicates  an  abnormal  intestinal  putrefaction 
with  absorption  of  deleterious  products." 

That  indican  in  the  urine  is  caused  by  abnormal  tissue  metabolism 
is  not  well  supported  by  evidence.^ 

It  is  found  in  carcinoma  and  chronic  peritonitis.  It  is  generally 
present  when  suppurations  are  in  progress;  probably  indol  is  absorbed 
from  the  focus  of  putrefaction.  The  ingestion  of  pus  from  pyorrheal 
pockets  in  the  mouth  may  easily  lead  and  has  led  to  chronic  gastritis 
and  intestinal  putrefaction,  in  which  latter  Bacillus  coli  communis 
plays  an  important,  assistant  part.  The  liver  may  be  disordered 
primarily,  thus  favoring  the  condition  owing  to  lessened  formation 
of  bile,  or,  secondarily,  owing  to  its  increased  function  as  a  poison 
destroyer.  The  intestinal  putrefaction  causes  the  formation  of  indol, 
etc.,  thus  leading  to  the  presence  of  indican  in  the  urine.  The  exces- 
sive use  of  proteid  food  not  only  overloads  the  intestine,  but  invites 
putrefaction  therein;  also,  the  amount  absorbed  being  excessive,  the 
eliminative  functions  are  overtaxed,  leading  to  disease. 

2.  Drug  Intoxication. — The  use  of  arsenic,  phosphorus,  or  other 
inorganic  poisons,  or  the  vegetable  alkaloids,  as  morphine,  cocaine, 
atropine,  etc.,  or  the  continued  contact  with  lead  salts,  all  undoubtedly 
affect  metabolism  some  beneficially  when  employed  in  suitable 
doses  in  diseased  conditions,  or  injuriously  in  continued  excessive  use. 
Thus,  atropine  in  small  doses  checks  secretion,  e.  g.,  of  the  salivary 
and  mammary  glands.  Phosphorus  continued  produces  fatty  degen- 
eration. 

3.  Bacterial  Intoxication. — The  toxic  products  of  bacterial  action 
(ai)art  from  tiie  aromatic  products),  as  the  ptomaines  and  albumoses 
(toxins),  act  as  ferments  upon  proteid  tissue,  causing  cellular  waste 
either  by  ferment  action  (destruction)  or  by  stimulation  of  the  cells, 
either  directly  or  through  the  nervous  system,  to  the  production  of 
antitoxic  substances  in  excess,  which  by  Ehrlich  are  claimed  to  be 
discharged  into  th(;  blood.  No  doubt  the  cell  is  also  rendered  less 
capable  of  anabolism.     (See  I^ateral  Chain  Theory.) 

This  is  seen  in  fevers  in  wliich  emaciation  (excessive  waste)  is 
f)rov('d  l)y  the  increased  output  of  urea. 

Intrinsic  Intoxication. — In  this  class  may  be  placed  all  intoxications 
jM-odiiccd  l)y  substances  originating  in  excess  within  the  body  proj)er 

'  Thompson's  Practical  Meilicine. 

^  Test  for  indif-an:  add  nitric  acid  to  urinR — .sli;ik(>  willi  flilonifcjini  .'i  hluisli  cold?-  i.s 
imparted  to  tlie  chloroform  on  standinK. 

'  Leatlies,  Problems  in  Animal  Metabolism. 


GEXKRAL  MALXUTRITIOX  03 

as  a  result  of  inetal)olic  clistiirl)ance,  resulting  from  disease  of  the 
nervous  eentres  controlling  nietaholisni  or  of  organs  which  fail  to 
perform  their  duty  of  elaboration  for  metabolism  or  eliminati(jn  or 
elimination  proper,  in  part  or  entirely.  In  some  cases  compensatory 
elimination  by  other  organs  occurs,  which  may  be  effectual  or  may 
lead  to  disease  of  said  organ  or  organs.  A  good  example  of  compensa- 
tory elimination  is  seen  in  health  during  sudden  changes  of  atmospheric 
temperature.  Thus,  on  the  warm  days  perspiration  is  free  and  elimina- 
tion by  the  urine  lessened;  the  avenue  of  elimination  is  largely  reversed 
on  the  cold  days.     These  intoxications  may  also  be  classed: 

Uremia. — In  this  there  is  a  retention  of  urea  (as  ammonium 
carbonate,  or  its  congeners)  in  the  system  which  should  be  eliminated 
in  the  urine.  The  body  cells  are  chronically  or  acutely  poisoned, 
according  to  the  degree  of  the  retention,  death  resulting  in  the  com- 
plete form.    Xepliritis  is  a  common  cause. 

Diabetes  Mellitus. — In  this  disease  probably  the  essential  lesion  is 
a  hyaline  degeneration  of  the  islands  of  Langerhans,  of  the  pancreas, 
or  injury  to  the  floor  of  the  fourth  ventricle  of  the  brain  (diabetic 
centre),  which  maybe  caused  by  even  strong  mental  emotion,  as  grief. 

Carbohydrate  assimilation  is  interfered  with,  an  increased  amount  of 
sugar  appears  in  the  blood  and  urine  (in  the  urine  termed  glyco.suria), 
and  the  cells  are  unable  to  appropriate  it.  Proteid  destruction  with 
increased  production  of  urea  occurs  (excessive  waste). ^  An  excess  of 
phosphoric  and  sulphuric  acid,  /9-oxybutyric  and  diacetic  acids  are 
formed  or  retained,  anfl  hyperacidosis  results. 

The  sugar  in  diabetes  is  probably  first  formed  from  carl)oIiydrates, 
later  from  proteids,  the  carbohydrate  radicals  being  prol)ably  disso- 
ciated in  the  proteid  disruption. 

Therefore,  ]:)atients  who  form  sugar  after  the  elimination  of  sugar 
from  the  diet  furnish  a  grave  prognosis.  The  chief  aim  in  the  treat- 
ment is  the  almost  entire  elimination  of  carbohydrate  food  or  proteid 
food  containing  glycogen."  All  cells  have  a  lessened  resistance  to 
bacteria,  as  shown  by  an  increased  tendency  to  pneumonia  and 
tuberculosis,''  and  a  similar  })redisp()sition  to  j)yorrhea  alveolaris  is 
probable. 

Symptoms. — Great  thirst,  fre(juent  micturition  (polyuria),  increased 
amount  of  urine,  the  excess  of  sugar  in  it,  indicated  by  high  specific 
gravity  and  analysis,  exce.ssive  appetite,  emaciation,  dyspeptic  symp- 

'  SteiiEel,  A  Tp.\t-hoi)k  nf  Patliology.  ''  See  Works  on  Practical  Medicine. 

^  Stengel,  A  Text-book  of  Palliology. 


94  DISTURBANCES  OF  NUTRITION 

toms,  hypochondriasis,  insomnia,  skin  diseases,  as  furunculosis,  are 
common.  The  glycosuria  in  diabetes  melHtus  may  account  for  the 
cervical  caries  seen  in  diabetics  by  introducing  a  factor  in  lactic  acid 
fermentation,  viz.,  glycogen  (starch).     (See  pages  76  and  78.) 

Peculiar  Intrinsic  Intoxications. — Without  question,  intense  emo- 
tion results  in  the  production  of  intrinsic  intoxicants  having  some 
influence  upon  metabolism.  A  most  notable  example  is  the  classic 
one  of  a  mother,  who,  shortly  after  intense  rage  at  an  insult,  nursed  her 
child  with  fatal  result  to  it.  In  another  case  a  child  was  poisoned  by 
the  milk  of  a  wet  nurse  who  spent  a  night  in  debauchery  (J.  Lewis 
Smith).  The  causes  were  of  slightly  difi^erent  classes,  the  modus 
operandi  much  the  same.  Intense  anxiety  also  has  a  disturbing 
influence.  The  nervous  influence  no  doubt  alters  metabolism,  and 
the  products  act  as  poison  in  a  degree  corresponding  to  their  amount. 

Acid  Intoxication. — Many  acids  may  be  accumulated  in  the  blood, 
producing  the  condition  known  as  hyperacidosis  or  general  hyper- 
acidity. The  accumulation  is  probably  the  result  of  an  increased 
production  by  metabolism  or  the  incomplete  reduction  to  urea,  etc., 
of  normal,  acid  cell  excreta.  The  condition  probably  arises  as  the 
result  of  gastro-intestinal  disturbances  or  altered  nerve  influence,  or  the 
failure  of  function  in  an  organ,  as  in  diabetes  in  which  acidosis  exists. 
The  acids  are  carbonic,  lactic,  sarcolactic,  sulphuric,  phosphoric, 
uric,  diacetic,  and  /5-oxy butyric.  The  symptoms  probably  result  from 
the  acidosis  rather  than  from  any  one  acid. 

Suboxidation  always  accompanies  the  condition.  Some  of  the 
acids  combine  with  the  alkaline  elements,  and,  therefore,  reduce  the 
normal  alkalinity,  while  the  acids  left  disturb  metabolism,  thus 
leading  to  further  disturbances.     (See  p.  87.) 

Gout. — Gout  or  podagra  is  a  recurrent  n  on -suppurative  arthritis 
associated  with  the  deposits  of  sodium  biurate  in  the  joints,  and 
often  with  constitutional  symptoms.  It  may  be  acute  or  chronic, 
by  some  thought  always  chronic,  with  occasional  acute  manifestation. 
It  is  largely  hereditary  or  the  result  of  inherited  tendency  to  luxurious 
and  indolent  life. 

The  excessive  rise  of  uric  acid  from  proteid  waste  is  held  to  be  the 
cause  of  the  presence  of  biurates  of  sodium,  as  mechanical  irritants 
to  the  joints,  in  which,  owing  to  increased  age  (thirty  or  over)  and  its 
tendency  to  lessened  use  of  joints,  a  sluggish  circulation  with  increased 
acidity  of  the  fluids  of  the  part  favoring  precipitation  is  established. 
The  salts  crystallize  in  the  synovial  tissue  and  excite  inflammation. 


a  EX  ERA  L  MA  LXU  TRITIOX 


95 


Fig.    52 


A  slight  excess  of  uric  ;icid  in  the  blood  is  sufficient  if  the  local  con- 
ditions are  as  stated.  Ebstein  claimed  that  degeneration  or  necrotic 
changes  in  the  tissues  cause  the  precipitation.  The  sluggish  circulation 
leads  in  this  direction.     (See  Venous  Hyperemia.) 

The  conditions  leading  to  a  rise  of  uric  acid  are  many: 

1.  Richly  cooked  foods,  especially  proteid  and  sugar,  with  wines. 

2.  Sedentary  life  combined  with  the  above,  or  overwork  and  under- 
feeding, with  the  use  of  malt  liquors. 

3.  Chronic  lead  poisoning. 

4.  Defective  elimination;  the  output  in  the  urine  is  lessened  just 
before  the  arthritis  and  increased  after  it  (Ilaig). 

Chronic  Gout. — After  an  acute  attack  in  one  joint  others  may  be 
attacked,  and  tophi  (concretions  of  sodium  biurate)  form  in  the  ear  or 
nasal  cartilages,  joints,  sheaths  of 
tendons,  etc.  In  some  cases  crepita- 
tion of  the  joints  may  be  felt  and 
heard.  The  joints  are  distorted  and 
enlargements  by  the  tophi  occur; 
the  skin  over  them  may  be  smooth 
and  shiny,  but  not  inflamed.  The 
neighboring  veins  are  prominent. 

ConMituiional  Symptoms. — Com- 
plications. —  Weakness,  anemia, 
cachexia,  digestive  disturbances, 
dvspepsia,  gastric  and  intestinal, 
with  constipation,  failing  nutri- 
tion, deformity,  inability  to  exer- 
cise, mental  irritation  and  dulness, 
granular  atrophic  kidney,  cardiac 
hypertrophy  and  dilatation  with 
arteriosclerosis,  chronic  gastritis, 
asthma,  bronchitis,  c(>rebral  or 
other  thrombosis,  sciatica,  eye- 
skin  lesions,  obesity,  diabetes,  cholelithiasis,  gravel,  and  vesical  cal- 
culi  (Thompson). 

Goutiness. — (Gouty  Diathesis). — This  is  the  inherited  or  accjuireil 
condition  underlying  the  acute  and  chronic  forms  of  gout,  or  a  ten- 
flency  to  gouty  symptoms  in  parts  other  than  the  joints,  as  the  vital 
organs,  skin,  and  nervous  tissues.  According  to  Ewart,  "in  its  func- 
tional aspect  it  is  due  to  the  abnormal  acidity  of  tissue  juices,  while  a 


Toplii  of  gout.     (Zeiglrr.) 


96  DISTURBAXCES  OF  XUTRITION 

delicacy  of  tissues  is  produced  or  inherited,  causing  increased  irrifa- 
hiliiy  and  lowered  resistance."  The  following  diseases  and  symptoms 
may  be  associated  as  results,  and  in  themselves  show  the  force  of 
[Michaels'  claim  for  a  general  hyperacid  classification  of  individuals 
with  these  symptoms. 

Vascular  System. — ^Arteriosclerosis,  an  increase  of  the  fibrous  ele- 
ments of  the  arterial  walls  and  indicated  by  their  thickening  and  the 
high  tension. 

This  induces  overwork  of  the  heart,  resulting  in  cardiac 
hypertrophy,  and  this  occurring  in  the  coronary  arteries  produces 
failing  nutrition  of  the  heart  and  myocarditis  with  appropriate 
symptoms. 

Respiratory  System. — Asthma,  emphysema,  and  obstinate  recurrent 
bronchitis;  bronchial  catarrh  in  the  young. 

Genito-urinary  System. — Uric  acid  sediment  with  hyperacidity, 
hematuria,  urethritis,  oxaluria,  albuminuria,  glycosuria  in  some  cases, 
menstrual  disorders,  and  uterine  and  ovarian  disturbances. 

Nervous  and  Muscular  Systems. — Neuralgias,  muscular  soreness, 
lumbago,  sciatica,  bursitis,  sore  heels,  hemicrania,  or  migraine, 
neurasthenia. 

Digestive  System. — ^Acid  dyspepsia,  acid  eructation.  Tongue  may 
show  glossitis  or  leukoplakia,  gingivitis,  suppurative  tonsillitis  (infec- 
tion added),  bilious  headaches,  chronic  gastritis,  colic. 

Skin. — Harsh,  dry,  tending  to  eczema,  pruritis,  urticaria,  erythema, 
acne,  pityriasis,  furunculosis,  herpes,  exfoliative  dermatitis,  perspira- 
tion acid.  Early  graying  of  hair,  alopecia,  nails  have  longitudinal 
striiB  and  are  brittle. 

Eyes. — Iritis,  glaucoma,  conjunctivitis.  Lesions  of  retinal  vessels, 
retina  and  optic  nerve,  keratitis  and  panophthalmitis. 

These  symptoms  vary  widely  in  different  subjects. 

The  chief  points  of  interest  to  the  dentist,  apart  from  diagnosis 
of  goutiness,  is  the  pccidiar  fis-sne  delicacy,  and  the  general  hyperacid- 
ity as  a  cause.  Without  doubt  this  form  of  auto-intoxication  (acidosis) 
in  some  cases  leads  to  thickening  of  small  arteries  in  the  pericementum, 
leading  to  endarteritis  obliterans,  as  shown  by  Talbot,  and  while 
not  the  only  form  of  chronic  gingival  irritation,  is  probably  one  cause 
predisposing  to  gingival  infection  leading  to  the  more  complicated, 
persistent,  and  icciirrcnt  forms  of  pyorrhea  alveolaris. 

It  may  be  regarded  as  established  that  goutiness  may  exist  and 
lead  to  "declared"  gout,  or  merely  act  as  a  chronic  tissue  irritant. 


GENERAL  MALNUTRITIOX  97 

Treatment. — The  accepted  medical  therapeutics  of  goutiness, 
which  lies  within  the  especial  province  of  the  dentist,  may  well  be  given 
here.^ 

Diet. — -Three  moderate  meals  a  day.  Eating  between  meals  to  be 
avoided.  Any  meat,  except  pork,  once  a  day  only;  fresh  fish,  eggs, 
lean  ham  or  bacon,  oysters  or  shell  fish  at  the  other  meals  if  desired; 
oatmeal,  hominy,  cornmeal,  cracked  wheat,  stale  bread  and 
crackers,  fresh  green  vegetables  and  potatoes,  leguminous  vegetables, 
apples,  oranges,  cream  or  other  cheese  as  proteid,  soups,  tea  and 
coffee  in  moderation,  custard  and  gelatin  preparations.  Alkaline 
mineral  waters,  or  plenty  of  plain  water,  before  meals  and  at  bedtime, 
or  the  tablets  of  lithium  citrate  or  bitartrate  may  be  taken  dissolved 
in  water.  To  be  avoided  are  much  meat,  sweet  dishes  and  con- 
fectionery, pastry,  fried  foods,  pickles,  spices,  curry,  cakes,  griddle 
cakes,  alcoholic  and  malt  liquors. 

Hygiene. — Brisk  exercise  in  the  open  air  to  increase  oxidation  and 
elimination  through  the  induction  of  perspiration,  and  Turkish 
baths  if  no  organic  disease  as  of  the  heart  and  kidneys  exists,  and  then 
only  as  advised  according  to  the  advance  of  the  disease.  Daily  cokl 
bathing  with  brisk  rubbing;  wearing  of  woollen  clothing.  Sea  bathing 
or  medicated  baths.  The  bowels  should  be  kept  freely  open  with 
cascara  sagrada  or  aloes  if  neeessarv. 

Special  Therapeutic  Indications. — For  anemic  and  neurasthenic 
cases.  Fowler's  solution,  with  iron  and  cod-liver  oil,  or  blood-making 
preparations. 

For  feeble  digestion: 

IJ — Tinet.  nux  voniic;c  tH  x 

Comp.  tinct.  gentian  or  ciiichinia f5J 

S. — Take  before  meals. 

For  constipation,  cascara  sagrada,  aloes,  Carlsbad  water,  thialion, 
a  laxative  salt  of  lithium. 

For  gastric  catarrh  with  constipation  and  high  vascular  tension: 

I^ — Sodium  sulpliafe 5 J 

S. — Take  in  a  lialf  tuiiihlorfiil  of   hot  water  one  hour  before  meals,  two  or  three  times 
a  day. 

For  persistent  high  vascular  tension: 

Nitroglvcerin gr.  '/lOO  every  three  hours. 

Or, 

Sodium  nitrate gr.  iij  three  times  a  day. 

Or, 

Choral  lijdrate gr.  v  three  or  four  times  a  day. 

'  Acknowledgment  in  part  to   Thompson's  Practical  Medicine. 

7 


98  DISTURBAXCES  OF  NUTRITION 

Lithemia. — This  is  a  condition  occurring  in  individuals  who 
overfeed,  drink  too  Htde  fluid,  exercise  httle,  and  are  under  various 
nervous  strains  or  overworked.  A  neurotic  disposition  and  stimulants 
enhance  the  disturbances  of  nutrition. 

Cold  weather,  adding  to  the  above  a  lessened  perspiration  and 
increase  of  work  by  the  kidneys,  increases  the  difficulty.  Tobacco  and 
alcohol  increase  the  ill  effects. 

There  may  be  no  symptoms  of  gout  in  even  marked  cases.  There 
is  acidosis  with  lithuria  (uric  acid  in  the  urine)  or  oxaluria;  eventually 
renal,  vascular,  and  hepatic  scleroses  develop,  together  with  liability 
to  localized  inflammation  chiefly  in  serous  membranes,  as  the  pleura 
or  synovia. 

The  hypothesis  is  that  uric  acid  or  some  proteid  toxin  irritates  the 
capillaries  to  contraction,  thereby  raising  vascular  tension,  and  by 
this  twofold  toxic  and  mechanical  action  causing  arteriosclerosis, 
which  in  turn  induces  cardiac  hypertrophy,  sclerotic  kidney  changes, 
and  vascular  hepatic  cirrhosis.     It  tends  toward  neurasthenia. 

Symptoms. — Nervous  Symptoms. — Vertigo,  tinnitus  aurium,  in- 
somnia, restlessness,  burning  or  pricking  sensation  in  the  palms  or 
soles,  darting  pains  in  the  limbs,  hebetude  of  mind,  hypochondriasis, 
hemicrania,  or  diffuse  basilar  or  frontal  headache,  general  nervous 
irritability. 

Digestive  Symptoms. — Lost  or  capricious  appetite,  coated  red 
or  dry  tongue  often  fissured,  aphthous  ulcers,  thirst,  metallic  taste 
in  the  mouth,  pyrosis,  hiccough,  gastric  oppression,  nausea,  gastralgia, 
vomiting,  flatulence,  constipation  or  irregular,  dark-colored,  frothy 
stool,  palpitation  of  the  heart  (an  hour  or  two  after  meals),  hepatic 
tenderness. 

Urine. — Scanty,  dark,  strongly  acid,  of  high  specific  gravity,  with 
often  brick-dust  sediment  of  urates.  Perhaps  temporary  albuminu- 
ria; perhaps  inflammation  of  urinary  passage. 

Skin. — Eczema,  pruritus,  urticaria  or  lichen. 

Treatment. — The  condition  of  life  should  be  reversed  as  to  previous 
eating  and  (hiiikiiig,  and  exercise  to  avoid  the  overstimulation  by 
proteid  food  waste  and  to  increase  elimination.  Stimulants  are  to 
be  avoided,  sodium  phosf)hate  given  for  its  action  upon  the  liver 
prom(iting  the  excretion  of  bile,  and  also  for  its  mildly  cathartic 
effect.  It  also  furnishes  an  element  for  regeneration  of  nervous 
tissue,  and  renders  the  body  fluids  more  alkaline.  Lithium  prepara- 
tions arc  of  little  value.     i*otassium  acetate,  bicarbonate,  and  citrate 


GENERAL  MALXUTRITIOX 


99 


arc  useful.     The  bowels  are  to  be  kept  open.     Ileadaelies  may  l)e 
relieved  by: 

I^— Phenacetin j?r.  xxxvi 

Salol, 

Caffeine aji     gr.  xxiv 

M.  and  ft.  capsiila-  No.   12. 

S. — A  capsule  three  or  four  times  a  day. 

For  the  neurastheuic  cases  treat  with  arsenic  and  glycerophosphates. 

The  diet  is  to  be  I'egulated  as  in  goutiness.  The  use  of  much  fat, 
meats  or  carbohydrates  is  to  be  avoided,  to  lessen  the  necessity  for 
oxidation  and  for  work  by  the  liver.  The  use  of  a  largely  vegetable 
diet,  to  render  the  body  fluid  more  alkaline.  Plenty  of  water  between 
meals,  to  flood  the  system.     Hygiene,  rest,  and  exercise,  as  in  goutiness. 

Rheumatism. — Rheumatism  is  an  acute  fever,  probably  of  infective 
origin,  characterized  by  constitutional  toxic  symptoms,  inflammation 
of  the  joints,  muscles,  serous  membranes,  skin,  or  even  tonsils.  It  may 
be  classified  as  acute,  chronic,  or  muscular  rheumatism. 

Etiology  of  Acute  Rheumatism. — It  may  be  transmitted  to  the 
newborn,  or  a  constitutional  tendency  to  it  may  b(>  inherited.  It  is 
most  common  to  young  adults  (fifteen  to  twenty-five  years),  l)ut  no 
age  is  exempt.     It  is  most  common  in  males. 

Climate,  exposure  to  cold,  injuries  and  overwork  of  parts,  occuj)a- 
tion  inviting  exposure  to  hardships,  chronic  alcoholism,  nervous  shock, 
debility,  starvation,  anemia  and  chorea,  are  other  predisposing  causes. 

The  exciting  cause  is  supposed  to  be  largely  due  to  a  bacillus 
isolated  from  the  blood  or  joint  of  rheumatic  patients,  but  it  is  also 
induced  by  a  diet  of  meat  or  the  fermentation  produced  by  overuse 
of  sugar  and  starches,  causing  a  rise  of  lactic  or  uric  acid  in  the  blood. 

Clinical  History. — It  presents  the  following  clinical  difference  from 
acute  ffout.^ 


Exciting  cause       .     , 
First  attack       .     .     , 
Later  attacks    . 
Appearance  of  joint  . 
Pain 

Subsidence    .     .     .     , 

Tophi   

Age  and  sex .     .     .     . 

I'^ffcct  of    trculnient. 


Acute  gout. 


Often  errors  in  eating  and  drinking. 
Commonly  in  one  great  toe. 
Both  toes,  tinners,  knees,  etc. 
Coh)r,  dark  red,  sliiny,  and  tense. 
Worse  at  niglit  or  early  morning, 

localized. 
Leaves  tliickeniiig  and  deformity 

with    repeated   attacks. 
In  lobes  of  ear,  finger-joint,  etc. 
Common  in  middle-aged  men;  very 

rare  in  chiUlren. 
Salicylates   have  but    little    effect; 

coh'liiiinu  marked  effect. 


Acute  rheumatism. 


Sometimes  cold  and  thinip. 

Commonly  in  large  joints. 

Hare  in  toes,  often  shoulder  or  hip. 

Lighter  red. 

Migratory  from  joint  to  joint. 

Leaves  normal  joints. 

Never  present. 

Common    in    young  persons,   diil- 

dren,  and  women. 
Salicylates     have    marked   effect; 

colchieum  no  effect. 


'  Thompson's  Practical  Medicine. 


100  DISTURBANCES  OF  NUTRITION 

S3nnptoms. — ^Pain  and  inflamriiation  of  joint,  which  may  be  pre- 
ceded by  headache,  indigestion,  constipation,  lassitude,  muscular 
aching,  chilliness,  mild  inflammation  of  tonsils,  pharynx,  and  larynx. 
Tongue  coated,  pale,  and  indented  by  the  teeth;  breath  foul.  Fever 
103°  or  104°  F. ;  sometimes  hyperpyrexia.  Sweating  during  the  height 
of  convalescence,  with  acid  odor  from  decomposition  of  fatty  acid, 
but  may  be  neutral  or  alkaline  in  parts  of  same  person,  therefore  not 
an  effort  at  elimination  of  acid. 

Saliva. — Acid,  excess  of  potassium  sulphocyanide. 

Urine. — Hyperacid,  urates  increased,  chlorides  diminished,  uric 
acid  abundant,  sometimes  albuminuria. 

Heart. — Pericarditis  and  endocarditis  in  one-fourth  of  all  cases. 

]\IiND. — Clear  except  in  hyperpyrexia. 

Skin. — Urticaria,  petechise,  ecchymoses,  purpura,  eczema  at  times; 
subcutaneous  nodules  in  youth. 

Complications. — Conjunctivitis  occasionally;  chorea  frequently. 

Prognosis. — Uncertain  as  to  period  before  recovery;  relapses,  or 
recurrence  common. 

Treatment. — Sodium  salicylate  and  oil  of  gaultheria,  internally, 
relieve  the  pains  and  inflammation.  Cold  baths  to  reduce  the  tem- 
perature. Blisters  as  counterirritants;  protection  from  jarring  by 
cotton  and  fenders;  guaiacol  with  glycerin,  oil  of  wintergreen,  etc.,  as 
local  lotions.     The  diet  is  much  the  same  as  in  gout. 

Chronic  Rheumatism. — This  form  has  much  the  same  etiology,  but 
is  more  common  after  the  fortieth  year.  It  appears  in  much-used 
joints,  and  is  most  common  in  females. 

Morbid  Anatomy. — Fibrous  thickening  and  contraction  produce 
moderate  thickening  and  distortion  of  joints;  atrophy  of  muscles 
about  joints  may  occur. 

Symptoms. — Symptoms  are  of  slow  onset;  general  health  good  unless 
inability  to  exercise  produces  alteration.  Pain  absent  except  when 
joint  is  overworked  or  in  damp  weather.  The  fingers  may  be  deflected 
laterally  and  flexed  by  contraction  of  tendons.  Febrile  attacks,  101°  F., 
occur  from  time  to  time,  but  the  urine  is  normal. 

Prognosis. — Disease  progressive,  no  recovery,  but  temporary  im- 
provement by  treatment  so  that  the  joints  may  remain  quiescent  for 
years.     Never  fatal. 

Systemic  Treatment. — Simjjle  alkalies  or  alkaline  waters,  arsenous 
acid,  ^77  gr.  t.i.d.,  cod-liver  oil  for  the  debilitated  and  anemic,  Carlsbad 
salts  or  sodium  phosphate  for  constipation. 


GENERAL  MALXUTRITIOX  ]01 

Local.— Dreiicliing  with  hot  (105°  to  1 10°  F.)  and  cold  (70°  F.)  water 
alternately,  followed  l)y  massage  and  wrapping  the  joint  in  flannel. 
Sweating  in  an  enclosing  box  with  hot  air,  240°  or  250°  F.,  followed 
by  Swedish  movements.  The  lotions  used  for  acute  rheumatism  are 
also  used.     The  diet  is  much  the  same  as  for  goutiness. 

Muscular  Rheumatism. — In  this  form  of  rheumatism  the  dis- 
turbance is  in  the  muscles,  with  little  constitutional  disturbance. 
The  essential  lesion  is  prol)ably  an  inflammation  of  the  muscles, 
though  the  nerves  may  suffer. 

Symptoms. — Local  tenderness  and  pain  increased  l)y  every  contrac- 
tion of  the  muscle.  Pain  stationary,  worse  by  night  and  during 
})arometric  disturbances;  oxaluria-in  some  cases. 

Scorbutus  (Scurvy). — ^This  is  a  subacute  or  chronic  disease, 
characterized  by  inanition,  anemia,  and  asthenia,  with  purpura  and  a 
tendency  to  swelling  of  the  gums. 

While  of  doubtful  origin,  defective  hygiene  and  the  use  of  improper 
foods,  especially  the  lack  of  fresh  vegetables  and  fruits,  and  the  use 
of  salted  foods,  the  improper  absorption  of  food  owing  to  chronic  intes- 
tinal maladies,  as  dysentery,  or  to  cachexias,  as  in  malaria,  cancer,  and 
syphilis,  are  the  chief  causes,  though  infection  has  been  held  to  act 
upon  those  debilitated  by  the  above  causes.  In  young  children  it 
is  due  to  the  use  of  proprietary  foods  instead  of  fresh  food,  and 
appears  mostly  from  the  eighth  to  the  twelfth  month,  rarely  before 
the  sixth  or  after  the  sixteenth  month. 

The  circulation  is  feeble  and  the  blood  impoverished. 

The  gums  are  red  and  swollen,  protrude  over  and  between  the  teetli 
if  present,  and  bleed;  the  breath  is  offensive,  owing  to  putrefaction  of 
the  blood. 

The  stomach  shows  great  irritability,  and  there  is  thirst  and  craving 
for  acid  foods. 

The  joints  are  swollen  and  painful,  owing  to  the  hemorrhages. 

The  urine  is  high  colored;  the  acidity  and  temperature  lowered. 

Treatment. — As  a  prophylactic  and  cure,  lime,  lemon,  or  orange  juice, 
together  with  the  use  of  fresh  vegetables  and  fruit  in  adults,  or  their 
juices  in  infants.  Fresh  milk  modified,  white  of  egg,  and  beef  juice, 
or  breast  feeding,  are  to  be  substituted  for  proprietary  foods  or  table 
feeding  in  infants. 

Rachitis  (Rickets). — This  is  a  disease  found  in  infants  devel- 
oping typical  deformities  in  the  bones,  and  due  to  a  deficiency  of  lime 
salts  in  them,  in  turn  probably  (hie  to  an  absorption  of  tliat  j)rcs(>nt, 


102  DISTURBANCES  OF  XUTRITTOX 

bv  hvperemic  tissue  present,  and  a  diminution  in  the  deposition  of  a 
fresh  supply.  There  is  usually,  also,  hypertrophy  of  the  liver  and 
spleen.  The  prolonged  lactation  of  the  child  upon  unfit  milk,  poor 
in  fat,  and  the  overuse  of  proprietary  foods  lacking  the  proper  food 
elements,  as  farinaceous  food  or  exclusively  a  condensed  milk  diet. 
The  teeth  develop  slowly  and  are  apt  to  be  of  faulty  structure.  The 
general  line  of  treatment  is  much  the  same  as  for  scorbutus. 

Neurasthenia. — This  is  a  condition  of  nervous  exhaustion,  no 
reserve  nerve  matter  being  held  for  even  slight  effort.  It  is  often 
accompanied  by  nervous  excitability,  insomnia  or  disturbed  sleep, 
apprehension,  melancholia,  failure  of  appetite,  and  feeble  digestion. 

Nervous  energy  is  lost  and  irritability  remains.  It  may  be  caused  by 
continued  excitement  or  overwork  of  the  nervous  system,  and  responds 
to  rest,  regulated  diet,  general  tonics,  treatment  by  glycerophosphates 
of  lime  and  soda  in  the  serious  cases,  while  in  mild  cases,  exercise  in  the 
open  air,  baths,  sea  or  mountain  air,  combined  with  the  tonic  treat- 
ment and  abstinence  from  stimulants,  effect  a  cure.^  In  view  of 
demonstrations  upon  animals  that  nerve  tissue  is  actually  used  up 
in  nervous  energy,  the  above  treatment  probably  permits  a  gradual 
restoration  of  the  elements  of  nerve  tissue. 

Oxaluria. — The  increase  of  sodium  and  calcium  oxalate  crystals 
in  the  urine  indicates: 

1.  That  food  rich  in  oxalic  acid  (as  tomatoes  or  rhubarb)  has 
been  used  in  increased  quantity. 

2.  That  intestinal  fermentation  is  existent  and  forming  it  from 
glucose  (Baldwin). 

3.  That  intrinsic  increased  production  of  oxalic  acid  by  oxidation 
of  uric  acid,  in  turn  derived  from  the  purine  bases  of  the  nucleins,  and 
nucleo-albumin  of  the  tissues  is  present. 

It  frequently  accompanies  the  increase  of  uric  acid  in  the  urine,  and 
is  regarded  by  Simon^  as  due  to  impairment  of  normal  oxidation  pro- 
cesses in  the  liver.  Thus  it  may  be  found  in  goutiness  and  lithemia. 
It  is  also  associated  with  dyspeptic  and  nervous  symptoms,  pro- 
ducing a  condition  known  as  oxalic  acid  diathesis.  It  also  sometimes 
accompanies  diabetes. 

Continued  oxaluria  may  result  in  the  formation  of  calcium  oxalate 
calculi.  It  is  frequently  associated  with  nervous  irritability,  hypo- 
chondriasis, and  neurasthenia.  Oxalates  are  found  in  the  urine  and 
saliva.    (See  p.  88.) 

'  See  Tliornpson'.s  Practical  Mpilicine.  '^  Clinical  DiiiKiiosis. 


GEXERAL  MALXUTRITinX  103 

Phosphaturia. — The  trihasic,  phosphoric  acid,  HgPO^,  is  a  normal 
product  of  iiictabolisni,  and  like  other  acids  combines  with  salts  before 
elimination.  Its  alkaline  combinations  are  sodium  phosphate, 
NajPO^;  calcium  phosphate,  ('a^iPOJ,;  and  magnesium  phosphate, 
Mg3(POj2,  which  may  also  be  found  in  alkaline  urine.  Its  neutral 
combinations  are  disodium  hydrogen  phosphate,  NajH-PO^;  calcium 
hydrogen  phos])hate,  CallPO^;  and  magnesium  hydrogen  phosphate, 
Alg.II.POj,  all  found  in  the  blood  and  in  neutral  urine.  Its  acid 
combinations  are  sodium  dihydrogen  j)hosphates,  NaHjPO^,  and 
calcium  dihydrogen  phosphate,  Ca(H2POJ^,  found  in  acid  urine,  and 
to  which  the  normal  acidity  is  partly  and  chiefly  due. 

Ammonium  magnesium  phosphate  (NII^MgPO^ +  01120)  or  triple 
phosphate  is  also  found. ^ 

^Nlany  of  the  ])hosphates  are  derived  from  the  food,  but  some  are 
formed  by  proteid  catabolism;  one-third  of  all  excreted  is  eliminated 
in  the  intestinal  secretion;  some  are  eliminated  in  the  saliva,  as  shown 
by  the  formation  of  salivary  calculi.  In  diseases  requiring  increased 
phagocytosis,  as  febrile  conditions,  the  elimination  of  phosphates  falls, 
the  phosphates  probably  being  utilized  in  the  formation  of  leuko- 
cytes. 

The  excretion  is  increased  in  diabetes  and  tuberculosis. 

A  very  large  increase  in  the  total  amount  of  phosphates  eliminated 
(7  to  9  grams  in  twenty-four  hours)  is  called  phosphatic  diabetes, 
and  has  been  associated  with  four  classes  of  symptoms: 

(a)  Cases  with  marked  polyuria  and  marked  nervous  symptoms. 

(6)  Cases  preceding  or  accompanying  pulmonary  diseases,  espe- 
cially tuberculosis. 

(c)  Cases  iii  which  phosphaturia  alternates  with  or  co-exists  with 
glycosuria. 

{d)  Cases  in  which  oxaluria,  ])olyuria,  and  slight  albuminuria  are 
present,  and  in  which  some  relationship  with  gout  exists.     (See  p.  8<S.) 

An  increase  in  the  amount  of  ])h()sphat('s  in  the  blood  tends  to  the 
production  of  calculi. 

As  nerve  tissue  contains  a  considerable  amount  of  lecithin  or  j)hos- 
phorized  fat  essential  to  it,  excessive  drain  upon  this  may  result 
in  a  loss  of  this  substance  by  catabolism,  with  loss  of  ])hosphates 
doubtless  masked  by  the  prepontlerance  of  phosphates  derived  from 
the  food. 

This  is  borne  out  by  the  IxMieficial  use   of    glycen)])hosphates  of 

'  Kirkcs"  PhysioloKv. 


104  DISTURBANCES  OF  NUTRITION 

lime  and  soda,  rest,  and  general  tonic  treatment  in  neurasthenia. 
(See  p.  102.) 

Albuminuria. — ^The  presence  of  albumin  in  the  urine  may  be 
either  (1)  transitory,  remittent,  or  cyclic  (recurring  with  regularity),  as 
the  result  of  functional  disturbances,  as  anemia,  adolescence,  in  general 
malnutrition,  after  severe  exercise  or  cold  baths;  or  (2)  due  to  organic 
disease  of  the  kidney,  as  acute  and  chronic  nephritis,  renal  arterio- 
sclerosis, and  amyloid  degeneration  of  the  kidney;  or  (3)  to  fevers,  as 
typhoid  and  yellow  fever,  and  is  due  to  the  presence  of  bacterial  toxin 
in  the  blood;  or  (4)  to  circulatory  disturbances,  as  organic  heart  disease, 
or  to  local  circulatory  disturbances,  as  compression  of  renal  veins  by  a 
pregnant  uterus;  or  (5)  to  impeded  outflow  of  urine;  or  (6)  to  hemic 
changes,  increasing  the  diffusion  of  albumin,  as  in  scurvy,  leukemia, 
pernicious  anemia,  jaundice,  and  diabetes;  or  (7)  to  toxins  in  the 
blood  other  than  febrile,  as  turpentine,  salicylic  acid,  phosphorus, 
arsenic,  etc.,  probably  producing  circulatory  disturbances  and  irrita- 
tion of  glandular  epithelium  of  the  kidneys;  or  (8)  to  neurotic  disturb- 
ances, as  epilepsy;  or  (9)  to  ingestion  of  excessive  amounts  of  cheese, 
eggs,  and  other  albuminous  food;  or  (10)  to  accidental  admixture 
after  urine  excretion  by  the  kidneys.^ 

It  is,  therefore,  like  oxaluria  and  phosphaturia,  more  a  symptom 
than  a  disease. 

'  Simon's  Clinical  Diagnosis. 


y^y/ 


a 


^#*SP? 


r/ 


??•., 


'^^4^' 


1    #' 


f 


y^y/7 


Ftff.vm. 


j/^l      ®       ^ 


BLOOD. 

(Elirlich  triple  stain.) 
(Prepared   by  Dr.  I.  P.  Lyon.) 

Fly.  I.     TYPES   OF    LEUCOCYTES. 

a.  Polymorphonuclear  Neutrophile.  6.  Polymorphonuclear  Eosinophile.  c.  Myelocyte 
(Neutrophilic),  d.  ."osinophilio  Myelocyte,  e.  Lnrge  Lymphocyte  (large  Mononuclear). 
/.  Small  Lymphocyte  (small  Mononuclear). 

Fig.  IL     NORMAL    BLOOD. 
Field  contains  one  neutrophile.     Reds  arn  normal. 

Fig.  III.     ANEMIA,   POST-OPER.ATIVE  (secondary). 

The  reds  are  fewer  than  normal,  and  are  deficient  in  haemoglobin  and  somewhat 
irregular  in  form.  One  normoblast  is  seen  in  the  field,  and  two  neutrophiles  and  on<3 
small  lymphocyte,  showing  a  marked  post-hsemorrhagic  anaemia,  \vith  leucoeytosis. 

Fig.  IV.     LEUCOCYTOSIS,   INFLAMMATORY. 

The  reds  are  normal.  A  marked  leucoeytosis  is  shown,  with  five  neutrophiles  and 
one  small  lymphocyte.  This  illustration  may  also  serve  the  purpose  of  showing  th3 
leucoeytosis  of  malignant  tumor 

Fig.  V.     TRICHINOSIS. 
A  marked  leucoeytosis  is  shown,  consisting  of  an  eosinophilia. 

Fig.  VI.     LYMPHATIC  LEUKEMIA. 

Slight  anaemia.  A  large  relative  and  absolute  increase  of  the  lymphocytes  (chiefly 
the  small  lymphocytes)  is  shown. 

Fig.  VII.     SPLENO-MYELOGENOUS    LEUK/EMIA. 

The  reds  show  a  secondary  anaemia.  Two  normoblasts  are  shown.  The  leucoeytosis 
is  massive.  Twenty  leucocytes  are  shown,  consisting  of  nine  neutrophiles,  seven  myelo- 
cytes, two  small  lymphocytes,  one  eosinophile  (polymorphonuclear)  and  one  eosinophilic 
myelocyte.  Note  the  polymorphous  condition  of  the  leucocytes,  i.e.,  theip  variations 
from  the  typical  in  size  and  form. 

Fig.  VIII.     VARIETIES   OF    RED    CORPUSCLES. 

a.  Normal  Red  Corpu.scle  (normocyte),  b.c.  Anaemic  Red  Corpuscles,  d-g.  Poikilocytes. 
A.  Microcyte.  i.  Megalocyte.  j-n.  Nucleated  Red  Corpuscles,  j.k.  Normoblasts  /.  Micro- 
blast.    m,n.  Megaloblasts. 


CHAPTER    V. 
DISTUllBANCRS  OF  THE  VASCUI.AR  SYSTEM. 

A  SUITABLE  amount  and  quality  of  blood  normally  flows  through  the 
circulatory  apparatus,  and  is  in  close  relation  to  processes  of  nutrition. 

The  amount  of  blood  in  the  vessels  may  be  increased  (plethora), 
though  not  permanently.  It  may  be  decreased  rapidly  in  quantity, 
as  by  hemorrhage,  or  its  red  corpuscles  may  be  gradually  lessened 
in  number  (acute  or  chronic  anemia).  The  proportion  of  white 
corpuscles  to  red  ones  may  be  increased  abnormally  (leukemia). 
The  hemoglobin  of  red  corpuscles  may  be  deficient  (chlorosis). 
Locally  the  amount  of  blood  in  a  part  may  be  increased  (hyperemia 
or  inflammation)  or  diminished  (ischemia). 

Normally  the  blood  contains  floating  in  the  plasma  5,000,000  red 
corpuscles,  or  erythrocytes,  and  from  5000  to  10,000  (1  to  500  red) 
white  corpuscles,  or  leukocytes,  to  each  cubic  millimeter.  (See  Plate, 
Fig.  II.)  A  marked  increase  in  the  number  of  erythrocytes  is  termed 
polycythemia;  a  marked  decrease,  oligocythemia.  The  temporary 
increase  in  number  of  white  corpuscles  is  leukocytosis;  a  persistent 
increase,  leukocythemia  or  leukemia. 

The  blood  corpuscles  may  be  classified  as  follows: 

See  Plate. 

Fig.  53   Fig.  VIII,  a 

f      Normal  to      f  i     •     n  ^    n    o    a 

,  ,      ,  <  Noniiocytcs  (normal  size;,  1,  2,  .3,  4.  a 

Erythropytes.  blood.  ( 

j  f  Microcytes  (small  size)  '• 

Pathological    J    Maorocytes  (large  size) 
I     indicators.      i   Megalocytes  (very  larg< 


Non-nucleated 
red  corpuscle-,. 


Megalocytes  (very  large  size)         ...  i 

{  Poikilocytes  (irregular  form)   .  .     d  e  f  g 


Erythroblasts. 

Nucleated  red  corpuscles   I     ,,     ,     >     -if  Normoblasts  (normal  size)       ....  j  k 

derived  from  red  marrow   I      .     ,.                  ■!    Microblasts  (small  .size) / 

r  1  I      iridicaton?.  ,,       ,,,.,,  ■     v 

or  boneo.                (^                               (^  Megaloblasts  (large  size) m  n 

See  Plate. 

Fig.  M  Fig.  I. 

f  Lymphocytes  (small)    ...      22  %     o  / 

Normal  to        J    Lymphocytes  (large)    .       .       .         G  "      0  e 

blood.             I   PolymoriJhonuclear  neutrophiles  70  "      7  « 

Le\ikocytes,                                               j^  Polymorphonuclear  eosinophiles     2  "      S  b 


While  corpus 


Path. .logical 
itidicali>rs. 


Ba.sophilic  leukocytes  or  most  celLs. 
Neutrophilic  myelocytes  from  bone-marrow 
Eosinophilic  myelocytes 


106  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

Fig.   53 


Normal  blood  (triaeid  stain):  1,  noinial  red  cell,  flatly  spread  and  evenly  stained;  2, 
normal  rouleau;  3,  normal  red  cells  varying  slightly  in  size,  thickly  spread,  showing  central 
clear  areas;  4-,  normal  red  cell,  of  slightly  altered  shape;  5,  lymphocyte,  medium  size; 
G,  large  mononuclear  leukocyte,  incurved  nucleus;  7,  polynuclear  neutioi)hile  leukocyte; 
8,  eosinophile  leukocyte.     Separate  nuclear  lobes.     (Schmaus  and  Ewing.) 


ANEMIA. 


Anemia  is  a  condition  in  which  the  blood  is  lessened  in  quantity  or 
partly  deprived  of  its  essential  constituents — ?*.  e.,  red  corpuscles  and 
hemoglobin — in  consequence  of  which  the  tissues  receive  less  oxygen, 
and  the  g(>neral  nutrition  is  impaired. 

Acute  Traumatic  Anemia  occurs  as  a  result  of  copious  hemorrhage. 
The  individual  becomes  temporarily  pale  and  weak.  The  arterial 
pre.s.sure  is  lessened,  the  circulation  slowed,  and  the  pulse  is  frequent 
and  small.  Recovery  is,  as  a  rule,  prompt,  the  water  being  first 
restored  and  later  the  corpuscles  being  regenerated.'  Frequent  hemor- 
rhages cause  the  blood  to  become  watery,  and  debility  results  from 
impaired  nutrition.      (Se(>  Plate,  Fig.  III.) 

'  Zicglcr,  (ieneral  Pathology. 


ANEMIA  107 

Symptomatic  Anemia. — A  (liniiiuition  in  tlie  iiuml)cr  oi  red  cor- 
puscles may  occur  as  a  result  of  pi'otracted  overwork,  anxiety,  study, 
or  long-continued  illness,  such  as  a  fever. 

The  number  of  red  blood  corpuscles  may  be  reduced  to  one-half  the 
normal  amount,  and  there  is  a  corresponding  debility.  The  condition 
may  disappear  with  appropriate  removal  of  the  cause. 

Chlorosis. — This  is  a  form  of  anemia  occurring,  for  the  most  part, 
in  girls  and  young  women,  and  characterized  by  a  great  deficiency  in 
the  hemoglobin  of  the  red  corpuscles  without  a  corresponding  reduc- 
tion in  the  number  of  the  red  corpuscles.  In  the  watery  blood  very 
small  red  corpuscles  (microcytes)  are  seen;  also  a  few  very  large 
ones  (macrocytes),  and  some  of  irregular  outline  (poikilocvtes).^ 
Myelocytes  are  occasionally  seen  (Stengel).  The  pathology  is  un- 
certain. If  prolonged,  th(>  red  corpuscles  may  sink  in  numbers  to 
.3  or  2  millions  per  cubic  millimeter  and  20  per  cent,  of  hemoglobin. 

Being,  as  a  rule,  readily  cured  by  a  course  of  iron,  it  is  inferred 
that  the  body  is  starved  of  iron,  an  essential  constituent  of  hemo- 
globin. It  is  often  associated  with  gastric  disturbances,  constipation, 
defective  hygiene,  and  irregular  habits,  which  a})parently  have  a  causal 
relation.  The  skin  and  mucous  membranes  are  pale  and  have  a 
slightly  greenish  tinge.-  In  recovery  the  number  of  corpuscles  is 
first  increased,  then  the  hemoglobin. 

Leukocytosis. — This  is  not  a  form  of  anemia,  but  a  temporary 
increase  in  the  number  of  multinucleated  leukocytes,  apparently 
derived  from  tlie  lymphoid  structures  of  the  body  in  response  to  some 
demand  for  leukocytes.  Thus,  it  occurs  after  a  full  meal,  in  the  later 
months  of  pregnancy,  in  acute  fevers,  in  tuberculosis,  and  in  conditions 
accompanied  by  suppuration.^  Its  presence  during  the  course  of 
surgical  ilisease  has  been  held  to  be  diagnostic  of  pus  formation* — e.  g., 
in  abdominal  surgery  from  8000  to  20,000  per  cu.m.  (See  Plate, 
Fig.  IV.) 

Leukemia. — Tveukenn'a  is  a  disease  characterized  by  a  considerable 
increase  in  the  number  of  white  corpuscles  of  the  blood,  by  a  diminu- 
tion in  the  number  of  the  rvi\  corpuscles,  and  by  enlargement  of  some 
of  the  lymphatic  organs.  The  proportion  of  one  white  to  ten  red 
corpuscles  is  common  (1  to  o  often,  occasionally  1  to  1).  The  spleen 
may  be  hypertrophied  (splenic  leukemia).  The  lymphatic  glands  may 
be  hypertrophied  (lymphatic  leukemia).    In  theselatter  cases  the  blood 

1  Cifon,  Pathology  ami  Moihi.l  Anatomy.      -    Il)iil. 

•■'  n)i(l.  *  Cabot,  Boston  Modical  and  SurRical  .loiirnal. 


108  DISTURBAXCES  OF  THE  VASCULAR  SYSTEM 

contains  an  excess  of  uninuclear  leukocytes.  It  is  rare  except  when 
combined  with  other  forms.  When  the  marrow  of  bones  is  hyper- 
trophied  (myelogenic  leukemia)  large  mononuclear  leukocytes  with 
neutrophile  granules  are  found^  (myelocytes),  and  the  lymphocytes 
and  polymorphonuclear  forms  are  increased.^  The  blood  contains 
toxic  substances  generated  by  the  destruction  of  leukocytes,  xanthin 
bodies,  and  acids  (lactic,  acetic).  The  urine  frequently  contains  an 
excess  of  xanthin  bases  and  lactic  acid.     (See  Plate,  Figs.  VI  and  VII.) 

Pernicious  Anemia. — This  is  a  comparatively  rare  but  generally 
fatal  disease,  characterized  chiefly  by  a  great  fall  in  the  number  of  red 
corpuscles  to  one  million  or  less  per  cubic  millimeter,  those  remaining 
being  altered  in  form  and  size  and  showing  evidences  of  degeneration. 
The  total  hemoglobin  is  reduced,  but  the  relative  amount  may  be 
increased.  Degeneration  is  shown  by  peculiarities  of  staining. 
Normal  red  corpuscles  (normocytes),  nucleated  red  corpuscles  (mega- 
loblasts),  large  nucleated  red  corpuscles  (gigantoblasts),  microcytes, 
and  poikilocytes  are  found.  The  blood  platelets  and  leukocytes 
are  somewhat  diminished.^  The  oxygen-carrying  power  is  markedly 
lessened  and  all  tissues  suffer  from  malnutrition.  The  power  of 
coagulation  of  the  blood  is  lessened.  Marked  fatty  degeneration  of 
the  heart  muscles  is  apt  to  occur*  as  well  as  fatty  changes  in  the  kidneys 
and  liver. 

The  causes  are  obscure,  but  gastro-intestinal  disorders,  intestinal 
parasites,  pregnancy  and  lactation,  hemorrhages,  malaria,  syphilis, 
tuberculosis,  and  infections  are  the  chief  causes  supposed  to  produce  it. 

Aplastic  anemia  is  a  severe  type  of  progressive  pernicious  anemia, 
in  which  the  bone-marrow  fails  to  develop  myelocytes  and  erythroblasts 
owing  to  lack  of  marrow  cells  (hypoplasia  of  bone-marrow). 


COAGULATION  OF  THE  BLOOD. 

The  blood  when  drawn  from  the  body  or  in  contact  with  a  wounded 
surface  or  injured  vessel  wall  undergoes  a  process  of  solidification 
called  coagulation.  This  is  due  to  the  splitting  up  of  the  fibrinogen 
ordinarily  in  solution  in  the  blood  into  a  globulin  and  fibrin.  The 
latter  takes  the  form  of  a  network,  in  the  open  spaces  of  which  the 
corpuscles  are  entangled  (Fig.  54).     The  formation  of  fibrin  is  brought 

'  Zifgler,  General  I'aDi.iloKy.  «  Stengel,  A  Text-hook  of  Patliology. 

2  Oeen,  Pathology  ari<l  lUoihid  Anatomy.  ••  Ibid. 


COAGULATION  OF  THE  BLOOD 


109 


al)out  by  the  activity  of  an  unorganized  ferment  (fibrin  ferment  or 
thrombin)  Hberated  by  injured  white  corpuscles.  For  the  production 
of  this  ferment  calcium  salts  are  necessary/     Coagulation  may  occur 

in  the  living  vessel,  as  a   throm- 
bus, or  in  the  interstitial  tissue,  as 
^  ^^^^'^7'W^'S,-^<^^f<-^^  in  inflammation  and  infarction. 


Fk;.  55 


Fig.  54 


Filjrin  filaments  ami  l)lo<)d  tablets:  .1,  net- 
work of  fibrin,  shown  after  washing  away  the 
corpuscles  from  a  preparation  of  blood  tliat 
has  been  allowed  to  clot;  many  of  the  fila- 
ments radiate  from  small  clumps  of  blood 
tablets.  B  (from  Osier),  blood  c()rpuscle.s 
and  elementary  particles  or  l)lo()d  tablets 
within  a  small   vein. 

Fig.  56 


A  tliroinbus  in  Iho  saphenous  \cin,  show- 
ing the  projection  of  the  conical  end  of  the 
Ihrondjus  into  the  femoral  ve.ssel :  <S',  saphe- 
nous vein;  T ,  thrombus;  C,  conical  end  pro- 
jecting into  femoral  vein.  At  v  r,  opposite 
the  valves,  the  thrombu.s  is  softened.  (Vir- 
chow.) 


Diagram  to  show  phenomena  of  venous 
thrombosis:  r  i',  valves  of  veins;  «?»,  primary 
thrombus  (white);  cdefn,  .secondary  white 
thrombi  connected  with  primary  white  throm- 
bus by  various  red  thrombi;  li,  piece  i>(  white 
thrombus  becoming  detached  by  blood  cur- 
rent.    (Green,  modified  fri>m  Thonia.) 


Thrombosis. — The  formation  of  tiu'ombi  or  clots  within  llie  hviug 
vessel  may  occur  in  the  heart,  arteries,  veins,  or  capillaries.  If  the 
blood  stream  be  somewhat  retarded,  an  increased  number  of  white 
corpuscles  and  blood  phitelets  occupy  the  peripheral  zone  and  adhere 
to  the  vessel  waU.      If  the  vessel  wall  be  injured,  the  blood  platelets 

'  Kirkes'  Physiology. 


no 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


become  attached  to  it.  With  these  platelets  the  white  corpuscles  and 
sometimes  the  red  become  deposited.  Fibrin  forms  and  the  corpuscles 
are  included.  The  thrombus  is  red  when  red  corpuscles  are  included 
in  it;  white  when  only  white  corpuscles  are  present.  The  causes  of 
thrombosis  are  these:  (1)  A  retardation  of  the  blood  current  at  some 
point  from  some  cause;  (2)  local  changes  in  the  walls  of  the  vessels 
and  probably  pathological  changes  in  the  blood. ^ 

Older  thrombi  are  firmer  than  those  recently  formed.  Thrombi 
are  also  formed  in  the  capillaries,  a  circumstance  which  favors  the 
spontaneous  cessation  of  hemorrhage.  They  may  form  in  the  vessels 
in  inflammation.     Remaining  in  the  situations  in  which  they  were 


Fig.  57 


Embolus  impacted  at  the  bifurcation  of  a 
branch  of  the  puhnonary  artery,  sliowing  the 
formation  of  thrombi  beliind  and  in  front  of 
it,  and  the  extension  of  these  as  far  as  tlie 
entrance  of  the  next  collateral  vessels:  E, 
embolus;  it'',  secondary  thrombi.     (Virchow.) 


a     V 

Diagram  of  a  hemorrhagic  infarct:  <i,  artery 
obliterated  by  an  embolus  (e);  c,  vein  filled 
with  a  secondary  thrombus  (th);  1,  centre  of 
infarct  which  is  becoming  disintegrated;  2, 
area  of  extravasation;  3,  area  of  collateral 
hyperemia.     (O.  Weber.) 


formed,  they  either  undergo  simple  or  puriform  softening  or  are 
calcified,  or  are  resorbed  and  replaced  l)y  connective  tissue.  (See 
Regeneration.)  The  calcified  varieties  are  called  phleboliths  in  the 
veins;  arteriolitlis  in  the  arteries.  In  senile  gangrene  a  thrombus 
may  extend  a  great  distance. 

Embolism. — Portions  of  the  softened  varieties  of  thrombi  may 
become  detached  and  float  about  in  the  blood;  these  are  called  (Mnboli. 
Other  foreign  substances  may  act  as  emboli — e.  (j.,  air  or  fat  glolniles. 
Jn  important  parts  it  may  caus(;  local  anemia,  necrosis,  or  slow  or 
rapid  death. 

If  the  thnjnibiis  l)e  septic,  as  in  the  case  of  puriform  softening,  the 


'  Zicglor,  (JciKTM-l  PallKiJogy. 


COAGULATinx  OF   THE   HLOOD  HI 

emboli  may  lodge  in  small  vessels  and  cause  secondarv  septic  disease 
processes,  as,  for  example,  in  the  cases  of.  pyemia  accompanied  by 
infarctions. 

Infarction. — When  an  embolus  occludes  a  terminal  artery,  that  is,  an 
artery  whose  branches  spread  like  those  of  a  tree  without  anastomosis, 
the  part  first  becomes  ischemic,  but  soon  the  backward  pressure  from 
the  vein  upon  the  blood  in  the  capillaries  causes  an  extravasation  of 
blood  into  the  interstitial  tissue  of  the  wedge-shaped  area,  forming 
what  is  called  a  hemorrhagic  infarct.  A  clot  forms,  degeneration  of 
the  clot  occurs,  and  if  aseptic  it  is  absorbed  and  replaced  l)y  connective 
tissue  (se*e  Regeneration);  if  caused  by  a  septic  embolus,  it  may  be 
involved  in  the  resulting  septic  process — e.  g.,  in  pyemic  metastatic 
abscess.  Infarction  has  been  held  by  Black  to  occur  in  the  dental 
pulp.  A  demonstration  has  been  made  by  Hopewell-Smith.  (See 
Diseases  of  the  Pulp.) 

Hemorrhage. — By  hemorrhage  is  meant  the  escape  of  blood  from 
the  vessels.  It  may  be  arterial,  venous,  or  capillary.  If  the  vessel 
is  ruptured,  it  is  hemorrhage  hy  rhexis.  If  it  occurs  by  diapedesis,  as 
in  infarction  (from  veins  and  capillaries  only),  it  is  hemorrhage  hy 
diapedesis.  The  diapedesis  occurs  through  the  capillary  wall  rather 
than  the  stomata;  pressure  is  the  cause.  Hemorrhage  usually  ceases 
sponfanrously  through  thrombosis. 

If  hemorrhage  occurs  into  the  tissues  it  receives  the  following 
designations,  the  escape  itself  being  called  an  effusion  or  extrava- 
sation : 

Ecchymosis,  an  effusion  of  moderate  extent  into  tissue  beneath  a 
surface,  as  into  subcutaneous  tissue. 

Petechia,  the  same,  but  small  and  circumscribed;  when  an  extensive 
area  is  involved  it  is  termed  a  suffusion. 

Infarction,  when  the  area  involved  is  that  supplied  by  terminal  and 
non-anastomosing  arteries. 

Hemorrhage  involves  an  injury  to  vessels  by  traumatism,  or  disease 
rendering  them  incapable  of  retaining  the  blood,  or  by  increased  press- 
ure, as  in  violent  exertion,  or  in  congestion  of  local  vessels,  as  in  venous 
hyperemia,  or  as  the  result  of  diminished  atin()s])heric  pressure,  as  in 
high  altitudes.  Tlie  extravasated  blood  corjiuscles  may  be  disinte- 
grated into  pigments  (see  p.  81)  and  be  absorbtul  or  deposited  in 
the  tissues,  as  in  a  bruise;  or  excite  inflammation  or  cyst  formation 
(extravasation  cyst).  Acute  hemorrhages  or  repeated  extravasations 
lead  to  anemia. 


112  DISTURBAXCES  OF  THE  VASCULAR  SYSTEM 

Hemorrhagic  Diathesis. — This  is  a  condition,  largely  hereditary,  in 
which  coagulation  does  not  close  wounds  readily,  and  ordinarily  trivial 
wounds  may,  in  spite  of  surgical  aid,  induce  death  by  hemorrhage. 
Hereditary  hemorrhagic  diathesis  (hemophilia)  is  usually  transmitted 
tlirough  the  female  to  the  male  descendants — i.  e.,  from  grandfather  to 
grandson  through  the  grandfather's  daughter — ^and  seven  or  more  gen- 
erations of  hemophilics  have  been  recorded.^  Males  suffer  more  than 
females  in  the  ratio  of  about  11  to  1. 

In  a  family  of  207  members,  in  four  generations,  37  were  hemo- 
philics, all  of  the  male  sex,  almost  half  died  from  hemorrhages  usually 
in  infancy,  w^hile  the  tendency  to  bleed  lessened  as  they  grew  older.^ 

According  to  Legg,^  "It  is  of  three  degrees  of  severity: 

"1.  Characterized  by  external  and  internal  bleedings  of  every  kind, 
and  by  joint  affections. 

"2.  By  spontaneous  hemorrhages  from  mucous  membranes,  but  no 
traumatic  bleeding  or  ecchymoses,  and  no  joint  affections. 

"3.  A  tendency  simply  to  ecchymoses.  The  first  is  seen  most  fre- 
quently in  men,  the  second  in  women;  the  third  may  appear  in  either 
sex." 

The  joint  affections  are  due  to  hemorrhage,  and  simulate  rheumatic 
affections.  Hemophilics  are  apt  to  be  thin-skinned,  neurasthenic, 
and  liable  to  sudden  flushings  and  vasomotor  disturbances.*  Blondes 
suffer  more  than  brunettes.^ 

The  injured  part  may  bleed  from  the  first,  or  a  normal  clot  may  form 
and  secondary  hemorrhage  or  capillary  oozing  occur.  Death  may 
rapidly  occur,  or  the  patient  bleed  to  fainting  or  until  almost  dead, 
and  hemorrhage  then  cease.  This  may  require  any  period,  even 
weeks. 

The  pathology  of  the  condition  is  uncertain.  Fillebrown''  reports 
a  fatal  case  in  wliich  the  arteries  were  excessively  thin.  Porter  points 
out  that  the  blood  may  clot  in  the  receptacle,  yet  not  in  the  small 
vessels  of  the  wound,  and  infers  that  some  hereditary  deficiency  exists 
which  interferes  with  the  action  of  the  vasoconstrictors. 

Hemophilics  usually  manifest  a  history  of  bleeding  before  puberty, 
and  hemophilic  infants  have  died  from  hemorrhage  due  to  gum- 
lancing,  circumcision,  etc.  The  therapeutic  measures  indicated  are 
hemostatics  internally,  local  styptics,  compresses,  etc.       Potassium 

'  Porter,  International  Dental  Jounuil,  1900.       ^  Losser,  International  Journal  of  Surgery. 

3  Musser,  Medical  DiaKno.sis.  ■*  Porter,  loo.  cit. 

'Thompson,  Practical  Medicine.  "  International  Dental  .Journal,  1900. 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION  113 

permanganate,  made  into  a  paste  with  vaseline,  is  recommended  as  a 
styptic. 

In  case  of  tooth  extraction  reimplantation  has  been  urged,  but  must 
be  done  under  aseptic  precaution  as  any  infected  dead  pulp  or  even 
a  root  infected  by  contact  with  the  hands,  saliva,  etc.,  may  substitute 
a  condition  almost  as  bad  as  the  hemorrhage. 

Sodium  sulphate,  gr.  iss,  every  two  hours,  has  been  of  service  in 
marked  hemorrhages.^ 

The  following  is  useful : 

I^. — Calcii  chloiidi gr.  Ixxv  to  cl 

Aquae  destillatce fjiiiss 

Syrupi  mentliise ov — M. 

Tablespoonful  doses  or  a  clyster  containing  75  grains  calcium  chloride  and  a  few  drops  of 
tincture  of  opium. ^ 

For  persistent  postextraction  hemorrhage,  Endelmann  has  recom- 
mended : 

I^. — Vin  ergotse,  U.  S f  3ij 

Sig. — Teaspoonful  every  two  hours. 

Dilute  sulphuric  acid,  hydrastis  canadensis,  calcium  chloride,  and 
gelatin  locally  and  by  injection.^  The  gelatin  may  contain  tetanus 
spores  and  should  be  sterilized  for  forty  minutes  or  longer  at  100°  or 
120°  C*  Suprarenal  extract,  gr.  xx  to  oj)  topically,  gr.  x  by  mouth 
every  four  hours,  is  also  useful.  Absolute  quiet  and  the  withholding 
of  food  for  two  days;  the  hunger  to  be  relieved  by  small  doses  of 
opium  and  thirst  by  ice-water  in  small  quantities.^  The  acute  anemia 
induced  requires  treatment. 

Individuals  known  to  be  hemophilic  should  live  a  hygienic  life  and 
avoid  all  injuries,  however  slight,  possible  to  avoid  in  the  hope  of  an 
eventual  outgrowing  of  the  condition.  If  operation  be  unavoidable 
they  should  be  treated  with  calcium  chloride,  gr.  iij  ter  die,  for  not 
more  than  four  days,  as  thereafter  the  coagulability  of  the  blood  is 
decreased.® 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION. 

The  amount  of  blood  in  a  part  may  be  increased  or  diminished. 
The  types  of  local  disturbance  of  the  circulation  differ  as  to  causes, 
phenomena,  and  effect,  and  as  to  the  indicated  treatment  for  each. 

'  Reverdin.  Dental  Cosmos,  February,  1904,  p.  1G2.  '  Rosod,  New  York  Med.  Jour. 

'  Hare,  Practical  Therapeutics.  *  Journal  Amer.  Med.  Assoc. 

'  Porter,  loc.  cit.  '  Hare,  loc  cit. 

8 


114  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

In  health  the  bloodvessels  are  maintained  at  a  proper  caliber  through 
the  action  of  two  sets  of  vasomotor  nerve  fibers : 

1.  The  vasoconstrictors,  which  control  the  involuntary  muscles  of 
the  vessel  wall  and  which,  when  stimulated,  cause  contraction  of  the 
vessel. 

2.  The  vasodilators,  which,  when  stimulated,  inhibit  the  muscular 
action  and  permit  dilatation. 

Ischemia. — ^This  is  local  anemia.  The  quantity  of  blood  in 
a  part  is  less  than  normal.  It  is  direct  when  some  cause  obstructs 
the  flow  from  an  artery  into  a  part,  as  when  pressure  of  any  sort  is 
applied  directly  to  a  part  or  to  the  artery  leading  to  it,  or  when 
an  injection  of  fluid  has  been  made  into  apart  as  in  cocaine  injections. 
Disease  of  an  artery  may  deprive  a  part  of  blood  as  in  thrombosis 
or  arteriosclerosis.  Anastomotic  circulation  may  eventually  relieve 
a  part,  if  not  it  remains  pale  and  cold,  atrophies  and  may  undergo 
degeneration  or  necrosis.     An  infarct  may  remain  ischemic. 

Arterial  Hyperemia. — ^Arterial  or  active  hyperemia  is  a  more  or 
less  prolonged  increase  in  the  amount  of  blood  in  the  dilated  arteries 
of  a  part.  It  expresses  the  reaction  which  occurs  as  the  consequence 
of  the  presence  of  an  irritant,  the  action  of  which  lessens  the  arterial 
tension  and  permits  dilatation  with  a  consequent  excess  of  blood. 

Causes. — ^The  lessened  arterial  resistance  is  produced  either  by  a 
stimulation  of  the  vasodilator  nerves  or  a  sedation  or  paralysis  of  the 
vasoconstrictor  nerves.  Certain  causes  act  to  produce  constriction  of 
the  vessels,  but  later  the  muscle  cells  of  the  walls  are  fatigued  and 
dilatation  results — e.  g.,  the  reaction  after  the  prolonged  application 
of  cold. 

The  removal  or  diminution  of  pressure,  to  which  vessels  have 
become  accustomed,  is  also  a  cause  of  their  dilatation;  often  sudden 
enough  to  cause  bursting. 

Irritants  and  mild  injuries  act  upon  the  sensory  nerves  of  a  part,  and 
by  reflex  action  through  the  vasomotors  (sympathetic  system)  produce 
hyperemia  of  the  part  itself — e.  g.,  heat. 

Irritation  of  sensory  nerves  may  induce  a  reflex  hyperemia  in  other 
parts  to  which  branches  of  the  same  nerve  are  distributed — e.g.,  the 
peripheral  hyperemia  of  neuralgia,  induced  by  irritation  of  a  tooth 
pulp. 

A  similar  effect  may  be  produced  in  deep-seated  organs  to  which 
other  nerves  are  distributed — e.  g.,  hyperemia  of  deep  organs  through 
the  application  of  irritants  to  the  skin  over  them  or  hyperemia  of  the 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION  115 

intestinal  wall  (tenth  nerve)  as  the  result  of  the  stimulation  of  a  pulp 
underlying  an  erupting  tooth  (fifth  nerve). 

Collateral  hyperemia  is  induced  by  the  diminished  flow  of  blood  to 
other  parts — e.  g.,  by  the  bandaging  of  parts  or  through  the  chilling 
of  the  surface  of  the  body.  A  part  having  a  lessened  resistance  may 
become  hyperemic. 

Compensatory  hyperemia  may  occur  through  the  removal  of  one  of 
a  pair  of  organs;  the  other  receives  the  excess  of  blood,  sometimes 
becomes  hypertrophied,  and  takes  upon  itself  an  increased  amount 
of  work.  (See  Hypertrophy).  A  physiological  hyperemia  occurs  in 
organs  during  periods  of  activity,  the  work  required  acting  as  a 
stimulus  to  the  vasomotor  nerves. 

Arterial  hyperemia  is  produced  as  the  first  step  in  the  process  of 
inflammation.     (See  Inflammation.) 

Pathology. — ^The  arteries  are  dilated;  there  is  an  increased  flow  of 
blood  through  them  and  also  to  them  through  their  own  nutritive 
arteries;  the  pressure  in  the  veins  rises  as  the  veins  are  enlarged  to 
accommodate  the  blood.  As  exudation  sometimes  does  not  increase 
markedly,  the  lymph  pressure  is  not  increased  except  in  marked  cases, 
in  which  some  edema  may  occur.  The  function  of  the  part  may  be 
disturbed  in  the  more  marked  cases.  (For  illustrations,  see  Hyper- 
emia of  the  Pulp. 

Results. — Continued  arterial  hyperemia,  as  a  rule,  results  in  an 
increase  of  nutrition.  The  arteries  may  be  permanently  enlarged,  their 
walls  thickened,  and  the  tissues  about  them  hypertrophied  in  con- 
sequence of  the  increased  capacity  for  work  in  the  part.  Hyperes- 
thesia of  nerves  and  nervous  tissue  is  often  a  result.  In  marked 
hyperemia  with  function  altered  there  is  a  tendency  to  the  degener- 
ations.    (See  Arterial  Hyperemia  of  the  Pulp.) 

Symptoms. — These  naturally  would  be  and  are  increased  redness, 
temperature,  and  sensibility;  more  or  less  throbbing  in  marked  and 
pathological  cases,  in  some  cases  swelling  and  throbbing  pain.  The 
increased  temperature  is  due  to  the  increased  oxidation. 

Degrees  of  Hyperemia. — It  is  to  be  borne  in  mind  that  the  hyper- 
emia may  be  of  several  grades,  varying  from  a  very  mild  exaltation  of 
function  and  sensation  to  a  distinctly  pathological  condition  with 
altered  function.  The  eft'ects  may  be  constructive  in  character  or 
destructive,  the  former  due  to  the  increased  nutrition,  the  latter  to 
interference  with  it.  (See  Constructive  and  Destructive  Diseases  of 
the  Pulp.) 


116  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

Hyperemia  as  a  Local  Predisposition. — It  is  generally  acknowledged 
that  the  presence  of  a  local  hyperemia  lessens  the  resistance  of  a  part 
to  the  action  of  pathogenic  bacteria — e.  g.,  hyperemia  of  the  lungs 
to  Bacterium  pneumoniae. 

Treatment. — The  principle  underlying  the  treatment  is  to  remove 
the  cause  and  procure  surgical  rest.  The  symptoms,  as  a  rule,  then  sub- 
side promptly.  It  may  be  that  the  conditions  require  treatment  irre- 
spective of  the  cause,  which  may  not  be  determined  or  be  absent,  the 
vessels  being  dilated  as  the  effect  of  a  previously  acting  cause.  The 
effect  aimed  at  is  the  reduction  of  the  dilated  vessels.  This  is  attempted 
at  times  through  the  use  of  drugs;  for  example,  ergot  stimulates  the  vaso- 
constrictor system  and  lessens  the  caliber  of  all  the  vessels,  including 
those  affected.  Aconite,  the  antagonist  of  ergot,  reduces  the  heart 
action  by  paralyzing  the  motor  apparatus  of  the  heart,  thus  reducing 
the  arterial  pressure.^  Less  blood  is  delivered  to  a  part  in  a  given 
time.  Many  cases  of  superficially  seated  hyperemia  are  amenable  to 
local  treatment. 

Local  sedation  of  sensory  nerves  and  contraction  of  vessels  are  pro- 
duced by  application  of  dry  or  wet  cold  (ice-bags,  ice  wrapped  in 
muslin,  cloths  taken  in  succession  from  a  block  of  ice,  etc.);  also  by  the 
application  of  sedative  astringents,  as  the  liquor  plumbi  subacetatis 
in  the  well-known  formula  of  lead-water  and  laudanum : 

I^. — Tincturse  opii f 5j 

Liq.  pivunbi  subacetatis f 5j 

Aquffl Oj — M. 

in  which  to  the  astringent  effect  of  the  lead  is  added  the  sedative  effect 
of  the  opium. 

The  principle  of  derivation  is  also  employed.  What  is  known  as 
counterirritation  is  a  common  means  of  treatment.  An  irritant  such 
as  a  mustard  plaster  or  a  blister  or  dry  cup  applied  at  a  distance  to  the 
affected  part  induces  a  flow  of  blood  to  the  point  of  application  and 
lessens  the  amount  of  blood  in  the  area  of  hyperemia.  The  volume 
of  the  blood  being  in  definite  amount,  if  an  excess  exist  in  any  part  a 
deficiency  will  be  found  in  other  parts. 

The  hot  pediluvium  acts  upon  this  principle  by  drawing  a  consider- 
able excess  of  blood  into  the  vessels  of  the  lower  extremities.  This 
action  is  increased  by  adding  a  small  quantity  (two  or  three  tablespoon- 
fuls)  of  mustard  to  the  hot  water.  It  is  suggested  by  Endelmann  that 
the  water  be  at  first  only  warm  and  the  hot  water  added  as  the  vessels 
relax.^ 

*  Biddle,  Materia  Medica  and  Therapeutics.  *  Dental  Cosmos,  1904. 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION 


117 


Fig.  59 


The  volume  of  the  blood  may  be  actually  reduced  and  a  derivative 
hyperemia  of  the  sweat  glands  be  produced  by  the  use  of  diaphoretics. 
Cathartics  lessen  the  blood  volume  and  cause  mild  h^'pcremia  of  the 
alimentary  canal.  Diuretics  act  in  a  similar  way  upon  the  kidneys. 
In  deep-seated  hyperemic  counterirritation  is  valuable  alone  or  con- 
joined with  other  forms  of  derivation. 

Venous  Hyperemia. — ^^^enous  (mechanical  or  passive)  hyperemia 
is  an  excess  of  blood  in  a  part  beginning  in  the  veins,  which  are 
dilated  in  the  hyperemic  area,  though  they  may  be  occluded  between 
it  and  the  heart. 

Causes. — 1.  Any  mechanical  interference  with  the  passage  of  the 
blood  through  the  veins  on  its  way  to  the  heart — e.g.,  the  action  of 
bandages,  tumors  pressing  on  veins,  thrombi  in  veins,  etc. 

2.  Insufficiency  of  any  of  the  mechanical  forces  aiding  the  propulsion 
of  the  blood  through  the  veins — e.  (7.,  diminished  cardiac  power  or 
valvular  insufficiency,  obstructions, 
dilatations,  or  rigidity  of  arteries; 
insufficient  muscular  contraction 
upon  or  valvular  incompetency  in 
veins,  or  lessened  or  excessive  tho- 
racic aspiration,  etc.  The  second 
class  of  causes  produces  a  collection 
of  blood  in  the  veins  and  a  conse- 
quent reduction  of  volume  in  the 
arterial  system. 

Pathology. — The  veins  are  di- 
lated, the  current  is  slowed,  and  the 
intravenous  pressure  is  increased, 
in  consequence  of  which  watery 
(serous)  exudations    occur  in    the 

parts  about  them  (edema).  For  the  same  reason  in  marked  cases 
diapedesis  of  red  corpuscles  may  occur,  and  their  hemoglobin  may  be 
dissolved  out  (hemorrhage  by  diapedesis).  The  blood  in  the  parts 
not  being  sufficiently  changed,  and  in  some  cases  in  a  state  of 
stasis,  there  is  a  less(Mied  food  su])])ly  and  waste  removal,  and  cell 
nutrition  suffers  accoi'dingly.  ^'ital  processes  are  lessened,  secretion 
is  diminished,  there  is  less  oxidation,  and  hence  less  heat  is  pro- 
duced and  less  work  is  done.  Fatty  degeneration,  atrophy,  and  in 
markedly  continued  cases  necrosis  may  occur.  Long  continued  venous 
hyperemia  with  great    intravenous  pressure  may  produce  dropsies. 


Venous  hyperemia  of  the  liver.  Two 
capillaries  near  central  hepatic  vein,  show- 
ing the  thickening  of  the  walls  and  the 
accumulation  of  red  blood  corpuscles  within 
them.      X  500.      (Green.) 


118     DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

If  the  walls  of  the  veins  are  weak  and  are  permanently  distended 
or  thicken  under  pressure  and  become  tortuous,  the  condition  is 
called  varicosity  of  the  veins  (varicose  veins).  The  exudate  of 
venous  hyperemia  differs  markedly  from  that  of  inflammation.^ 

Hyperemic  Exudate.  Inflammatory  Exudate. 

Poor  in  albumin.  Rich  in  albumin. 

Rarely  coagulates  in  the  tissue.  Usually  coagulates  in  the  tissue. 

Contains  few  cells.  Contains  numerous  cells. 

Low  specific  gravity.  High  specific  gravity. 

Contains  no  peptone.  Contains  peptone  (product  of  cell  disintegration) . 

This  is  probably  due  to  an  increased  permeability  in  the  vessel  wall 
in  inflammation  permitting  the  albumin  of  the  blood  to  pass  through. 

Treatment. — ^The  treatment  consists  of  the  removal  of  the  mechanical 
obstruction  to  the  return  of  the  blood  and  mechanical  support  of  the 
engorged  vessels,  with  a  view  to  recovery  of  the  tone  of  their  muscular 
walls.  This  latter  is  accomplished  by  means  of  elastic  bandages  or 
compresses,  and  in  situations  in  which  these  cannot  be  used  astringents 
may  be  employed.  The  part  is  elevated,  when  possible,  to  aid  in  the 
return  of  the  blood  to  the  heart.  In  certain  circumstances,  as  in  an 
engorged  tooth  pulp,  actual  depletion  of  the  engorged  part  must  be 
resorted  to  by  bloodletting.  (See  Destructive  Diseases  of  the  Pulp.) 
In  cases  due  to  failure  of  blood-propelling  forces  these  are  to  have 
appropriate  treatment. 

INFLAMMATION. 

Inflammation  may  be  defined  as  a  series  of  hyperemic  changes 
expressive  of  the  reaction  of  living  tissue  to  irritation  and  char- 
acterized chiefly  by  an  excessive  diapedesis  of  leukocytes  and  exudation 
of  coagulable  lymph  from  the  bloodvessels. 

Causes. — ^Any  irritant  or  injury  capable  of  producing  a  lesion  of  the 
bloodvessel  wall  not  involving  its  immediate  death  can  produce  inflam- 
mation. In  case  direct  death  is  produced  the  inflammation,  if  any, 
occurs  in  the  tissue  contiguous  to  the  dead  part. 

The  causes  of  inflammation  may  be  divided  first  into  non-septic 
and  septic  or  infective.  The  non-septic  causes  may  be  extrinsic  or 
intrinsic.  The  extrinsic  non-septic  causes  are:  (1)  Physical  irritants, 
such  as  violence,  mechanical  irritation,  pressure  or  traumatism,  exces- 
sive heat  or  cold,  and  electrolytic  action.  (2)  Chemical  irritants — e.  g., 
the  action  of  acids,  caustics,  etc.     (3)  Nervous  or  vital  irritants — 

'  Park's  Surgery, 


INFLAMMATION  119 

e.  g.,  rubefacients,  epispastics,  arsenic,  etc.  These  act  only  on  living 
tissue  through  the  medium  of  the  nerves. 

An  intrinsic  non-septic  cause  may  produce  inflammation — e.g., 
urates  in  tissue,  mechanical  strains  upon  tissue,  temporary  lack  of 
blood  in  a  vessel  or  central  nervous  disturbance,  as  in  herpes  from 
locomotor  ataxia. 

Non-septic  causes,  as  a  rule,  produce  only  such  mild  inflammatory 
phenomena  as  are  concerned  in  circumvallation  of  an  irritant,  ab- 
sorption of  it,  and  in  repair  or  production  of  new  tissue.  No  pus  is 
produced  unless  pyogenic  bacteria  gain  ingress.  This  class  of  inflam- 
mation is  termed  simple  inflammation. 

Septic  or  Infective  Causes. — These  are  fungi  or  their  products, 
and  the  classes  of  inflammations  produced  are  much  more  severe,  con- 
tinuous, and  destructive  in  their  nature,  and  are  termed  infective 
inflammations. 

Pathology  of  Simple  Inflammation. — If  to  the  web  of  a  frog's  foot 
tincture  of  capsicum  be  applied  or  if  its  mesentery  be  exposed  to  the 
air  and  either  be  examined  under  the  microscope  while  the  animal  is 
living,  it  is  noted  that  after  a  possible  short  period  of  contraction  of  the 
arterioles  dilatation  of  arteries  at  once  begins  and  is  gradually  followed 
by  dilatation  of  the  veins  and  capillaries.  This  continues  to  steadily 
increase  for  about  twelve  hours.  During  the  first  hour  of  this  period 
the  blood  current  is  accelerated  and  arterial  hyperemia  may  thus  be 
said  to  be  the  first  stage  of  an  inflammation.  Following  this  accelera- 
tion the  blood  flow  is  increasingly  retarded.  The  retardation  is  due  to 
the  action  of  the  leukocytes,  large  numbers  of  the  mononuclear  and 
polymorphonuclear  forms  of  which  fall  out  of  the  central  blood  stream 
into  the  periaxial  stream  and  collect  along  the  walls  of  the  small  veins 
(Fig.  60,  b).  Several  layers  of  leukocytes  may  thus  form.  Probably 
some  peculiar  attraction  exists  between  the  leukocytes  and  the  wall  of 
the  vessel,  or  a  positive  chemotaxis  exists  as  in  infective  inflammation. 

This  massing  of  leukocytes  compels  the  red  corpuscles  to  the  centre 
of  the  stream  (Fig.  60,  a)  and  their  passage  is  mechanically  interfered 
with,  thus  the  further  dilatation  of  the  vessel  becomes  a  process  of 
venous  hyperemia.  The  vessels  are  increased  in  size  and  length  and 
become  more  tortuous.     Pulsation  is  noted. 

Coincident  with  retardation  of  the  blood  flow,  the  leukocytes  are 
seen  to  work  their  way  by  an  ameboid  movement  through  the  walls 
of  the  veins  and  to  some  extent  of  the  capillaries  into  the  perivascular 
spaces — i.  e.,  into  the  adjoining  tissue — in  which  they  may  move  far 


120 


DISTURBAXCES  OF  THE  VASCULAR  SYSTEM 


from  their  point  of  escape  and  mass  about  the  irritant  if  one  be  present. 
This  process  is  called  diapedesis  or  emigration  (Fig.  60,  e).  At  the 
same  time  a  fluid  rich  in  albumin,  and  thus  capable  of  coagulation, 
escapes  by  the  same  route  into  the  tissue  (Fig.  61).  Some  red  cor- 
puscles also  escape  (Fig.  60,  c.) 

As  the  venous  hyperemia  increases  the  flow  of  red  corpuscles  in  the 
veins  is  increasingly  retarded  until  stopped,  when  a  to-and-fro  motion 
(oscillation)  begins.  Finally  all  motion  ceases,  diapedesis  ceases,  and 
stasis  is  complete.  This  blood  may  remain  fluid  in  the  vessel  for 
several  days  (i.  e.,  without  coagulation),  and  if   the  blood  flow  be 


Fig.  60 


Small  vein  in  mesentery  of  dog,  after  exposure  for  half  an  hour  and  irrigation  with  salt 
solution:  a,  red  corpuscles;  b,  leukocytes  adhering  to  wall  of  vein;  c,  red  corpuscles;  d,  leuko- 
cytes which  have  escaped  from  vessel;  e,  leukocyte  in  act  of  escaping;  /,  fibrous  tissue.  X  340. 
Modified  from  Thoma.     (Green.) 

reestablished  the  separate  red  corpuscles  are  seen  one  by  one  to  roll 
away  from  the  general  mass  until  all  are  in  movement  and  stasis 
ceases  (Thoma). 

Coagulation  (thrombosi.s)  may,  however,  occur  in  the  vessels 
involved  in  the  stasis  and  the  part  be  later  removed  through  the 
process  of  resorption.  (See  Resorption  of  Clot.)  With  the  inflam- 
mation fully  established  there  are  in  the  tissue  the  following  elements: 
(1)  Leukocytes  and  some  red  corpuscles  and  lymphocytes  from  the 
tissue  lymphatics.  (2)  CoagulaJjle  lymph.  (3)  Later  new  em- 
bryonic cells  formed  by  mitosis  from  preexisting  connective-tissue  cells 
which  surround  the  leukocytes  massed  about  the  irritant.     These 


INFLAMMATION  121 

are  fibroblasts  ready  to  form  scar  tissue — i.  e.,  they  are  the  elements 
composing  granulation  tissue. 

The  disposition  of  these  elements  of  inflammation  is  as  follows: 
The  leukocytes  mass  about  the  irritant,  exert  a  certain  amount  of 
phagocytic  activity  (ferment  action),  and  may  in  turn  be  injured, 
liberating  fibrin  ferment,  which,  acting  upon  the  fibrinogen  of  the 
lymph,  produces  fibrin,  which  in  turn  forms  a  coagulum.  This 
coagulum  blocks  the  lymphatic  vessels  leading  from  the  part  involved, 
thus  causing  a  retention  of  fluid  in  the  tissue. 

In  the  later  stages  of  non-infective  inflammation  the  tissue  cells 
undergo  multiplication,  forming  cells  larger  and  having  more  power 
of  ameboid  movement  and  phagocytosis  than  the  leukocytes.  These 
become  mingled  with  the  leukocytes  in  the  area  of  inflammation.  They 
are  fibroblasts  from  which  all  the  connective  tissues  develop,  and  to 
the  action  of  which  regeneration  is  mainly 
due.     Around  and  about  the  focus  of   in-  ^^:^^ 

flammation  the  bloodvessels  are  in  a  con- 
dition  of   arterial  hyperemia   and    about  ~^' 
this  is  an  area  of  normal  tissue.     These       ' 
areas    shade  ofl'  into    each    other.     The 
phagocytes  cause  dissolution  of  coagula 
and  dead  aseptic  tissue,  and  remove  them. 

yp       ,  .      .  ,1  ,  ■        .       .  Iiiflamiiiatury    edema  of    skin. 

It     the     irritant     be     thus     removable     it     is        The    large     spaces     shown    were 

eaten  away.     If  the  dead  tissue  be  super-     ^''^^  ,^'t'*  ^^"''^^  fl"'*^-     ^  2.5. 

.  .  ...  (Boyd.) 

ficial,  the  connection  with  the  living  ti.ssue 

beneath  is  eaten  through  and  the  latter  thrown  off.  If  the  superficial 
tissues  have  been  previously  removed,  the  wound  is  covered  with 
the  exudates  and  leukocytes,  which  dry  into  a  scab,  beneath  which 
regeneration  occurs.  If  inflammation  occur  in  a  mucous  surface,  the 
exudate  and  corpuscles  escape  from  the  submucous  tissue  between 
the  epithelial  cells  as  a  catarrhal  discharge  (Fig.  62).  If  the  inflam- 
matory exudate  be  highly  coagulable  and  coagulate,  firm  swelling  is 
caused,  apt  to  lead  to  organization  of  tissue,  hence  called  fibrinous 
inflammation.  If  it  be  productive  of  hypertrophy,  it  is  called  pro- 
ductive inflammation.  If  the  exudate  be  watery,  poor  in  albumin, 
and  hence  not  readily  coagulable,  the  inflammation  is  called  serous 
inflammation. 

In  the  later  stages  of  simple  inflammation  the  coagula  are  dissolved, 
the  leukocytes  undergo  fatty  degeneration,  and  both  are  absorbed, 
together  with  such  tissue  as  has  undergone  liquefaction.     The  lym- 


122 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


phocytes  and  embryonic  cells  push  into  the  area  and  regenerate  the 
tissue.     This  is  the  phenomenon  of  resolution. 
Symptoms  of  Simple  Inflammation.     These  are: 

1.  Redness  due  to  the  excess  of  blood  in  the  vessels  and  in  the  tissue. 
In  some  cases  the  part  may  have  a  dusky  hue.  The  color  is  deepest 
in  the  area  of  greatest  stasis. 

2.  Heat  due  to  the  increased  oxidation  in  the  area  of  hyperemia 
about  the  area  of  stasis.  It  has  been  shown  that  there  is  no  increased 
heat  in  the  area  of  stasis.     In  this  area  chemical  action  is  lessened. 


Fig.  62 


Acute  bronchial  catarrh:  passage  of  leukocytes  through  the  epithelium  of  the  bronchus 
between  the  ciliated  cells.      X  700.     (Thoma.) 

3.  Swelling  due  to  the  excess  of  blood  in  the  vessels,  the  exudates  of 
leukocytes  and  fluid,  and  the  multiplication  of  tissue  cells.  The  hard- 
ness of  a  swelling  is  due  to  coagulation  of  the  fluid  exudate. 

4.  Pain:  the  result  of  the  pressure  of  the  effusion  upon  sensory  nerve 
terminals;  it  is  frequently  throbbing  in  correspondence  with  the  heart 
beat;  the  impulse  causes  temporarily  increased  pressure  upon  the  nerve 
terminals.  Gravitation  also  increases  the  pressure  and  pain  in  a 
dependent  part — e.g.,  in  a  hand  or  foot  or  in  recumbency  in  case  of 
pulpitis  (which  see). 


INFLAMMATION  123 

5.  Impaired  function  is  an  evident  result  of  a  disturbance  involving 
such  pathological  phenomena  as  have  been  described.  The  part 
cannot  be  used  owing  to  pain  and  stiffness  due  to  the  swelling,  also 
nutrition  of  any  part  being  impaired  it  loses  its  normal  function. 

There  are  no  general  disturbances  in  simple  inflammation  beyond  a 
slight  traumatic  fever  due  to  absorption  of  some  aseptic  material  from 
the  seat  of  inflammation — e.  g.,  fibrin  ferment.^ 

Infective  Inflammation, — If  microorganisms  enter  the  tissue 
through  a  wound  or  puncture  or  an  a})raded  surface,  or  if  they  locate 
upon  predisposed  or  non-resistant  mucous  membrane,  their  multi- 
plication causes  irritation  and  inflammation  of  the  tissue  about  them. 
This  at  first  resembles  a  simple  inflammation,  but  later  becomes 
more  severe,  prolonged,  and  may  spread  into  the  surrounding  tissue, 
or  in  some  cases  cause  inflammation  in  another  place  in  no  way 
connected  with  it  except  by  the  blood  or  lymphatic  channels  (metas- 
tasis). Briefly,  the  process  may  be  described  as  beginning  with  the 
entrance  or  location  of  the  organisms  and  their  multiplication.  An 
injury  of  the  vessel  walls  and  degeneration  of  some  tissue  occur 
and  the  phenomena,  such  as  occur  in  simple  inflammation,  begin. 
There  is  arterial  hyperemia,  later  retardation  of  the  blood  current; 
diapedesis  of  leukocytes  occurs,  and  a  copious  exudate  of  coagulable 
lymph  is  poured  out  into  the  intervascular  tissue.  By  positive 
chemotaxis  the  leukocytes  are  attracted  to  the  bacteria,  surround 
them,  and  apparently  endeavor  to  limit  their  activity,  or,  perhaps,  to 
digest  them.  If  the  bacteria  be  few  in  number  and  not  too  virulent,  the 
phagocytes  are  successful  and  the  phenomena  of  resolution  occur.  If, 
however,  the  contrary  be  the  case,  the  leukocytes  are  overcome  and  the 
inflammation  spreads.  In  case  of  much  toxin  formation,  negative 
chemotaxis  occurs  and  phagocytic  phenomena  are  held  in  abeyance. 
The  central  or  most  involved  area  dies.  It  is  thus  seen  that  there 
may  be  two  terminations  of  an  infective  inflammation,  resolution, 
and  necrosis. 

Resolution. — If  the  phagocytes  destroy  or  wall  up  the  bacteria,  so 
that  they  die  in  their  own  products  or  are  killed  by  the  protective 
juices  of  the  part  (alexins),  the  phagocytes  undergo  fatty  degeneration, 
the  lymphatics  are  unblocked,  the  circulation  is  reestablished,  the 
tissue  that  has  died  is  removed  by  resorption  and  replaced  by  scar 
tissue  if  the  loss  be  considerable.  No  evident  pus  nor  externally 
evident  necrosis  is  produced,  and  the  part  exhibits  phenomena  much 

'  Green's  Pathology  anil  Morbid  Anatomy. 


124 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


like  those  of  a  simple  inflammation.     This  is  the  only  termination 
for  a  simple  (non-infective)  inflammation. 


Fl  :.  (i3 


6-.' 


Miliary  abscCHS  in  a  case  of  septic  embolism  of  the  kidney:  a,  leukocytes  advancing  toward 
and  surrounding  (b)  a  mass  of  cocci,  in  whose  neiKhhorhood  all  trace  of  structure  has  disap- 
peared; c,  renal  epithelium  too  damaged  by  bacterial  products  to  take  the  stain;  d,  kidney 
tissue  staining  normally;  e,  vein  from  which  leukocytes  are  making  their  way  to  the  com- 
mencing abscess.      X  100.     (Green.) 


Necrosis. — Deatl)  of  a  part  may  result  from  infective  inflammation, 
either  with  or  without  pus  formation. 


INFLAMMATION  125 

Suppuration. — If  the  irritant  in  the  tissue  consist  of  pyogenic 
organisms,  such  as  the  Staphylococcus  pyogenes  aureus  or  albus,  the 
Streptococcus  pyogenes,  the  Bacillus  pyocyaneus.  Bacillus  typhi 
abdominalis,  Bacterium  pneumoniae,  or  the  Gonococcus,  pus  will  be 
formed,  provided  the  germs  be  not  killed  out.  The  Staphylococcus 
pyogenes  aureus  is  most  frequently  the  organism  infecting  wounds. 
It  is  practically  universal. 

Entering  a  part  the  bacteria  distributed  in  the  tissue  act  as  irritants 
and  excite  the  phenomena  of  inflammation  as  described.  Some  of  the 
cocci  are  taken  up  by  the  fixed  connective-tissue  corpuscles,  the  leuko- 
cytes, and  the  endothelial  cells  of  the  capillaries,  and  some  lie  free  in 
the  tissue.  The  cocci  multiply  and  the  polymorphonuclear  and  eosino- 
phile  leukocytes  increase  in  number  by  diapedesis  and  surround  them. 
The  original  tissue  cells,  including  those  of  the  bloodvessels,  undergo 
coagulation  necrosis  as  the  result  of  the  action  of  bacterial  ferments  and 
do  not  take  up  staining  reagents  (Fig.  63).  Coagulation  of  the  exu- 
dates occurs.  The  leukocytes  and  tissue  cells  are  in  part  degenerated 
into  pus  corpuscles  by  the  action  of  the  luiorganized  ferments  of  the 
bacteria — i.  e.,  their  nuclei  are  fragmented  and  they  undergo  fatty 
degeneration.  Some  cocci  die.  The  exudate  is  peptonized  into  a 
fluid  which,  together  with  the  cocci,  dead  leukocytes,  and  tissue 
remnants,  constitutes  'pus.  About  this  pus  is  a.  circumvallating  wall 
of  living  leukocytes,  and  about  this  again  a  zone  of  fibroblasts  arranged 
about  new  capillary  loops  (granulation  tissue).  The  whole  consti- 
tutes, when  confinetl  within  tissue,  an  abscess.  When  upon  a  surface 
the  granulation  tissue  is  upon  the  under  side  only,  and  the  whole 
constitutes  a  suppurating  ulcer. 

While  the  leukocytes  may  overcome  the  bacteria,  the  reverse  is  often 
the  case,  and  the  pus  cavity  enlarges  in  the  same  maimer  as  at  first  by 
a  new  formation  of  coagulation  necrosis,  more  circumvallation,  further 
liquefaction  of  the  coaguhim,  etc.  The  path  offering  the  least  vital 
or  mechanical  resistance  is  usually  followed  until  the  surface  of  the 
body  or  some  internal  cavity  is  reached.  The  last  portion  of  tissue 
overlying  the  forming  pus  is  tumefied  and  a  soft,  yellow  spot  appears. 
This  is  called  pointing.  The  tissue  is  ruptured  by  the  internal  pressure 
and  the  pus  escapes.  The  tract  from  the  ])oint  to  the  abscess  cavity 
is  Si  fistula.  As  soon  as  this  occurs  granulation  tissue  springs  up  upon 
the  sides  of  the  abscess  cavity  and  usually  soon  fills  it  with  scar  tissue. 
(See  Regeneration.)  If  the  cause  continue  to  act,  as  for  example,  in 
case  of  a  portion  of  dead  and  septic  bone  beneath  soft  tissue,  a  gan- 


126 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


grenous  pulp  in  a  tooth  root  or  infected  crypts  of  the  abscess  walls,  the 
granulation  tissue  breaks  down  and  the  condition  is  one  of  ulceration 
or  a  chronic  abscess  with  a  fistula.  If,  in  the  course  of  abscess  forma- 
tion, bone  be  encountered  by  the  pus,  it  may  be  and  often  is  molecu- 
larly  broken  down  into  pus.  (See  Acute  Apical  Abscess.)  It  does 
not  always  happen  that  the  pus  finds  escape  either  naturally  or  through 
surgical  aid:  the  patient  may  die  before  this  occurs,  or  the  tissues 
around  the  seat  of  pus  formation  may  form  a  boundary  wall  which 
the  organisms  fail  to  break  down  and  thus  die  starved  out.  The 
abscess  contents  undergo  changes  resulting  in  caseation,  or  later  the 
mass  may  calcify.  (See  p.  75.)  The  Streptococci  pyogenes  may 
multiply  laterally,  following  the  subcutaneous  cellular  tissue,  and 
produce  violent  spreading  inflammation  with  but  little  pus  formation — 
e.  g.,  some  forms  of  apical  abscess  and  erysipelas. 

Fig.  64 


^i^"  m 


An  abscess  in  the  skin.  The  horny  layer  has  largely  disappeared,  and  the  Malpighian  layer 
is  pushed  upward  by  the  subjacent  abscess  (a).  The  mass  of  pus  corpuscles  is  just  breaking 
down  to  form  a  cavity,  the  walls  of  which  are  thickly  infiltrated  with  similar  cells.     (Boyd.) 

The  products  (toxins)  from  an  abscess  or  infective  inflammation 
may  find  their  way  into  the  blood  and  a  general  toxemia  result,  or  the 
organisms  themselves  may  enter  the  blood  and  a  general  infection 
result  (septicemia).  There  are  various  varieties  of  pus  which  have 
names  describing  the  chief  characteristics : 

Creamy  pus  is  the  erroneously  called  laudable  pus  associated  with 
an  acute  abscess  or  ulcer  which  progresses,  as  a  rule,  toward  a  cure. 
It  is  of  a  yellowish-white  color,  creamy  consistency,  and  without  odor. 

Curdy  pus  contains  flakes. 

Ichorous  pus  is  thin,  odorous,  and  irritating. 

Mucopus  is  pus  containing  mucus. 

Seropus  is  pus  containing  much  serum. 

Sanious  pus  contains  blood. 


INFLAMMATION  127 

Cause. — The  cause  of  suppuration  is  the  development  in  tissues  of 
pyogenic  organisms.  The  action  of  these  causes  is  favored  by  the 
presence  in  the  part  of  a  hyperemia  or  simple  inflammation,  such  as 
the  injury  introducing  the  organisms  may  cause.  These  as  well  as 
depraved  or  debilitated  tissues  favor  the  action  of  bacteria — i.  e.,  act 
as  predispositions. 

Symptoms. — The  symptoms  of  suppuration  are  both  general  and 
local. 

Local  Symptoms. — The  symptoms  of  inflammation,  redness,  heat, 
pain,  and  swelling  occur,  but  usually  much  aggravated.  The  pain  is 
often  of  a  lancinating  character,  sudden  darts  often  following  com- 
parative quiescence.  On  the  other  hand,  the  throbbing  pain  may 
be  continuous  and  intense,  especially  when  the  pus  is  confined  by  bone 
or  tense  tissues,  as  in  case  of  a  felon  or  acute  apical  abscess.  Recalling 
that  around  the  pus  area  there  is  one  of  active  inflammation,  and 
about  that  hyperemic,  then  normal  tissue,  one  may  judge  of  the  degree 
of  involvement  of  deeper  parts  by  the  appearance  of  the  surface  above 
them.  Thus,  for  example,  hyperemia  at  the  surface  indicates  in- 
flammatory action  directly  beneath,  with  a  pus  cavity  still  deeper, 
while  inflammation  at  the  surface,  together  with  hardness  and  tume- 
faction, shows  a  more  involved  condition  of  the  tissue  directly  beneath 
it — i.e.,  a  more  advanced  state  of  inflammation  or  even  of  suppu- 
ration. 

The  softening  of  the  apex  of  the  swelling  gives  a  feeling  of  lessened 
resistance,  indicating  pointing  or  pus  at  the  surface.  In  large,  super- 
ficial abscesses  the  sensation  known  as  fluctuation  may  be  obtained  by 
placing  one  finger  on  one  side  of  the  swelling  and  gently  tapping  upon 
the  other.  Yellowness  of  the  apex,  together  with  softness,  indicates 
that  the  abscess  is  about  to  discharge  its  contents.  A  fistula  upon  the 
surface  is  indicative  of  a  discharged  abscess,  and  leads  to  a  pus-forming 
area  beneath  (chronic  abscess). 

General  Symptoms. — If  toxemia  be  produced  there  may  be  chills, 
and,  at  the  same  time,  fever  as  high  as  104°  F.  A  full,  bounding  pulse 
accompanies  this,  the  patient  is  constipated,  has  a  coated  tongue,  is 
exhausted  by  loss  of  sleep  and  often  disturbed  nutrition  due  to  the 
pain.  Here  may  be  other  evidences  of  septic  intoxication,  which 
may  become  profound.     (See  Septic  Intoxication.) 

Leukocytosis  after  surgical  disease  is  considered  pathognomonic 
of  suppuration  the  count  running  up  to  15,000  or  20,000  per  cubic 
millimeter. 


128 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


Ulceration. — ^The  development  of  microorganisms  upon  a  free 
surface  causes  tissue  degeneration  and  death,  as  described  under 
Abscess. 

Numerous  forms  of  pathogenic  organisms  are  capable  of  causing 
tissue  degeneration  and  death  of  a  mucous  or  skin  surface.  If  infection 
take  place  through  a  hair  follicle,  or  if  organisms  develop  upon  an 
abrasion,  or  in  the  epithelium  in  conditions  of  general  or  local  debility, 
the  epithelium  is  destroyed  over  an  area,  and  in  the  subepithelial  tissues 
the  organisms  multiply  and  cause  tissue  loss.  If  the  organisms  be 
pyogenic — and  ulcerous  surfaces  are  usually  infected  by  these  bodies — 
pus  is  formed  (Fig.  65).  Under  some  conditions,  as  in  debilitated 
and  neglected  children,  the  ulcerous  process  may  spread  rapidly,  as  in 
the  cheek  in  cancrum  oris;  or  when  specific  bacilli,  which  excite  much 
swelling  and  quick  death  of  the  tissues  of  the  cheek,  proliferate, 
causing  the  condition  called  noma. 

Fig.  65 


sr 


o 


luberculous  ulcer  of  the  Hitc^tii  c     a    mucf   a    &    submueo'^a    c   mu  culaii      j    ulcei 
t  tubeicle  in  the  muco'^a    t    focus  caseating  in  the  middle       X  12 

Prognosis. — Abscesses  tend,  as  a  rule,  to  spontaneous  cure  without 
marked  systemic  disturbance.  If  the  pus  discharge  persist  after 
evacuation  of  the  abscess,  persistence  of  the  cause,  or  infection  of  the 
abscess  walls  through  reinfection  or  by  retention  of  bacteria  in  the 
crypts,  is  to  be  suspected.  The  occurrence  of  rigors  (chills)  and  high 
fever  is  a  danger  signal.  A  fluttering,  weak  pulse  and  clammy  extrem- 
ities indicate  profound  septic  intoxication,  and  are  indications  for  local 
disinfection  and  systemic  treatment. 

Treatment  of  Inflammation. — If  the  cause  of  inflammation  be  in 
evidence  it  must  be  removed;  good  examples  of  removable  causes  are 
a  splinter  in  the  flesh,  a  gangrenous  tooth  pulp,  etc.  Ordinarily  the 
pus  of  an  abscess  or  an  ulcer  contains  the  cause  (bacteria)  within  it; 
therefore  the  pus  should  be  removed  by  opening  the  abscess,  if  its 
situation  can  })e  determined,  after  which  the  pus  cavity  is  syringed  out 


INF  LAMM  A  TION  1 29 

with  germicides,  which  destroy  the  pus  and  the  organisms.  Hydrogen 
dioxide  in  3  per  cent,  aqueous  solution  is  commonly  used;  it  is  made 
more  effective  by  the  addition  of  mercuric  chloride  (1  to  1000). 

In  ulceration  the  pus  and  organisms  are  destroyed  in  a  similar 
manner,  though  at  times  sloughing  tissue  requires  removal  by  the 
curette,  caustic  agents,  or  by  digesting  agents,  as  caroid,  papoid, 
brewers'  yeast,^  etc. 

Dead  bone  acts  as  a  septic  irritant  and  requires  removal,  and  at 
times  an  abscess  will  remain  persistently  infected,  requiring  surgical 
removal  of  tissue.  The  abscess  or  ulcer,  if  protected  from  further 
infection,  usually  heals  by  formation  of  granulation  tissue.  A  deeply 
seated  abscess  may  require  to  be  packed  with  antiseptic  gauze  (noso- 
phen),  in  order  that  it  may  granulate  from  the  bottom  out,  otherwise 
a  small  orifice  may  heal  permitting  a  re-collection  of  pus  beneath. 

Ulcers  are  usually  dusted  with  antiseptic  powders,  iodoform,  aristol, 
or  nosophen,  which  cause  drying  of  the  surface  and  prevent  the  access 
or  action  of  organisms.  Under  certain  circumstances  the  presence  of 
suppuration  is  not  certain,  though  phlegmonous  (spreading)  inflam- 
mation is  somewhat  pathognomonic  of  it.  In  such  cases  hot,  moist 
applications,  such  as  hot  poultices,  soften  the  surface  above  the  abscess 
and  determine  its  direction  of  discharge,  thus  limiting  burrowing. 
Counterirritants  applied  directly  above  the  inflamed  area  also  hasten 
in  such  cases.  The  stimulation  may  aid  resorption  (destruction  by 
phagocytosis)  of  the  pus  and  resolution  occur. ^  The  vascular  engorge- 
ment in  an  inflamed  part  may  be  reduced  by  local  bloodletting. 

Nancrede  found,  on  dividing  a  vein  upon  the  distal  side  of  an  area 
of  inflammation,  that  after  a  brief  period  the  flow  of  blood  was  estab- 
lished through  the  inflamed  area.  Local  blood-letting  by  leeches 
(Gensmer)  produced  even  more  marked  effects.  Drugs  which  stimu- 
late the  vasoconstrictors  (ergot),  and  those  which  paralyze  the  con- 
strictors (aconite),  lessen  the  blood  pressure  in  the  inflamed  area;  so 
that  if  administered  in  the  early  stages  of  inflammation  they  may 
modify  its  severity.  If,  on  the  contrary,  they  are  administered  after 
stasis  occurs,  they  increase  the  stasis — ergot  actively  and  aconite  pas- 
sively. If  the  flow  of  blood  through  the  inflamed  area  be  reestablished 
by  local  blood-letting,  then  the  arterial  sedatives  are  distinctly  useful 
in  lessening  the  flow  of  blood  to  the  part. 

When,  owing  to  vascular  engorgement,  throbbing  pain  is  a  promi- 
nent symptom,  applications  of  cold  are  useful  in  lessening  the  caliber 

»  Park's  Surgery.  '  Ibid. 


130      DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

of  vessels  and  in  relieving  pain.  But  if  there  be  firm  exudation  and 
marked  stasis,  cold  is  a  detriment.  Heat  then  gives  relief  through 
inducing  a  more  free  flow  of  blood  in  the  collateral  circulation.  Very 
hot  applications  act  as  do  cold  applications,  by  causing  contraction  of 
vessels,  and  may  be  used  to  abort  an  inflammation. 

In  certain  situations,  as  in  case  of  an  inflamed  tooth  pulp,  sedative 
applications,  antiphlogistics,  are  required.  Conjoined  with  local 
measures  of  reducing  vascular  engorgement,  the  use  of  counterirritants 
and  general  derivatives  are  indicated.   (See  Treatment  of  Hyperemia.) 

General  sedatives  are  at  times  demanded  for  the  relief  of  pain. 
Morphine  used  in  small  and  continued  doses  not  only  relieves  pain, 
but  causes  a  contraction  of  small  vessels.  Other  anodynes  are  also 
used  in  this  connection,  as  acetanilide.  Quinine  and  salol  are  useful 
as  correctives  of  the  intestinal  disturbance.  (See  Acute  Apical 
Abscess.) 

REGENERATION    OF    TISSUES. 

Connective  tissues  that  have  been  lost  by  inflammatory  process  or 
operation  are  replaced  by  granulation  tissue  arising  by  mitotic  division 
of  cells  of  the  connective-tissue  group.  The  forms  of  healing  are  by 
first  intention,  second  intention  or  granulation,  healing  under  a  scab, 
and  healing  under  a  clot.  Epithelial  tissues  are  replaced  only  by 
multiplication  of  epithelial  cells.  The  forms  of  healing  are  practically 
alike  by  formation  of  granulation  tissue,  the  form  being  simply  a  modi- 
fication (of  extent)  of  healing  by  second  intention. 

Healing  by  Second  Intention. — Shortly  after  evacuation  of  pus  from 
an  abscess  the  process  of  repair  is  instituted.  The  leukocytes  come  to 
the  surface  of  the  wound  in  great  numbers;  some  of  these  may  degen- 
erate into  pus  cells.  Immediately  beneath  the  uninjured  connective- 
tissue  cells  multiply,  forming  embryonic  cells  (fibroblasts) ;  at  the  same 
time  the  endothelial  cells  of  the  capillaries  multiply  at  points,  throwing 
out  solid-pointed  projections  or  buds  from  the  sides  of  the  capillaries 
(Fig.  66,  b).  These  lengthen  and  join  buds  from  other  capillaries 
(Fig.  66,  c,  d,  e).  By  mitosis  the  nuclei  divide  horizontally,  lying  side 
by  side  (Fig.  66)  d).  Later  these  separate  into  two  cells,  discovering  a 
lumen  into  which  blood  enters  from  the  parent  capillary  (Fig.  66,  a',  c). 
In  this  manner  loops  are  formed,  about  which  the  fibroblasts  are 
arranged  (Figs.  67  and  68). 


REGENERATION  OF  TISSUES 


131 


Together  these  form  minute  red  elevations  upon  the  surface  of  the 
abscess  cavity  or  wound,  called  granulations.  Repeated,  the  process 
gradually  fills  the  abscess  cavity. 


Regeneration  of  capillary  bloodvessels:  o,  normal  capillaries;  b,  capillary  process;  c,  new 
capillary  appearing  in  divided  process;  d,  process  undergoing  division;  e,  connecting  cell  in 
which  no  sign  of  division  has  yet  appeared.     Diagrammatic.     (Green.) 


P^iG.  67 


A  granulating  surface:  a,  layer  of  pus;  b,  granulation  tissue  with  loops  of  bloodvessels; 
c,  commencing  development  of  the  granulation  tissue  into  a  fibrillated  structure.  X  200. 
Diagrammatic.     (Rindfleisch.) 


132 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


Naturally,  collapse  of  the  walls  or  apposition  of  cut  edges  of  a  wound 
lessens  the  amount  of  granulation  tissue  necessary;  hence,  in  the  latter 
case,  healing  by  first  intention  (with  a  minimum  amount  of  granulation 
or  scar  tissue). 

The  wound  having  been  filled  up,  epithelium  grows  from  the  sides 
and  covers  the  granulations  (Fig.  69,  e).     The  granulation  tissue,  at 

Fig.  68 


Transverse  section  of  granulation  tissue  from  an  open  wound  with  fibropurulent  deposit: 
a,  granulation  tissue;  b,  fibropurulent  deposit;  c,  bloodvessels.      X  150.     (ZicRler.) 

first  highly  vascular,  later  contracts,  and  many  vessels  are  obliterated 
so  that  it  becomes  whiter  than  normal  tissue. 

The  indifferent  embryonic  cells  may  have  the  function  of  forming 
any  of  the  connective  tissues.  If  cartilage  is  to  be  formed,  chondrifi- 
cation  takes  place  about  the  specialized  cells.  If  l)onc  is  to  be  formed, 
certain  cells  form  islets,  al)out  which  calcification  proceeds.  Nerves 
require  a  month  or  more  to  pierce  the  cicatricial  tissue  (Eichhorst).^ 

1  Ziegler,  General  Pathology. 


REGENERATION  OF  TISSUES 


133 


In  healing  beneath  a  scab  the  exudation  and  leukocytes  upon  the 
surface  of  the  wound  dry  into  a  scab  beneath  which  granulations 
and  an  epithelial  covering  are  formed.  Later  the  scab  falls  off.  If 
prematurely  lost  the  granulations  are  exposed. 

In  healing  under  a  clot  the  clot  is  invaded  by  leukocytes,  which  have 
a  solvent  action  upon  it.  Granulation  tissue  forms  upon  all  sides  of  it, 
grows  into  it,  and,  at  the  same  time,  removes  it  by  resorption  (Fig.  70). 


Fig.  69 


Laparotomy  wound — sixteentli  day:  a,  eiiithelium;  b,  coriuiii;  c,  subcutaneous  fat;  rf, 
vessels  in  scar  tissue  of  corium;  e,  newly  formed  epithelial  layer;  /,  vessels  in  subcutaneous 
scar  tissue.      X  40.     Modified  from  Ziegier.     (Green.) 


If  the  clot  become  septic  the  granulations  may  become  infected  and 
break  down,  as  scar  tissue  in  its  early  vascular  stages  is  of  but  feeble 
resistive  power,  though  it  does  not  absorb  toxins  (Park). 

Healing  under  a  clot  is  the  form  commonly  seen  after  tooth  extrac- 
tion. 

In  certain  cases  of  abscess  with  contracted  fistula*  or  openings  of 
discharge,  the  orifice  may  close  before  the  granulations  have  filled  the 
pus  cavity.  If  pus  or  an  excess  of  exudate  be  now  formed  within  the 
cavity,  a  second  discharge  may  occur.     To  obviate  this  diflSculty, 


134 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


abscesses  are  often  packed  with  antiseptic  gauze,  so  that  healing  may 
occur  from  the  bottom  of  the  cavity,  while  drainage  is  assured.     In 

other  cases  the  placing  of  a  tent 
^^°-  "^^  or   drain    tube    in    the    fistula 

together  with  asepsis  suffice  for 
Q,  j    j^^  the  attainment  of  the  object. 

INFLAMMATION  OF  BONE. 

"Active  inflammatory  changes 
may  occur  in  the  periosteum, 
the  medullary  canal,  the  med- 
ullary spaces  of  the  spongy 
bone,  and  the  Haversian  canals, 
the  compact  tissue  and  ground 
substance  remaining  passive."^ 
The  inflammation  is  termed 
periostitis,  osteomyelitis,  and 
osteitis,  the  terms  referring  to 
the  point  of  location  of  the  in- 
flammation —  i.  e.,  the  peri- 
osteum, the  medulla,  and  the 
spaces  —  the  bone  being  in- 
volved in  all  cases.  Inflamma- 
tion of  bone  may  be  non-infec- 
tive or  infective;  the  latter  is 
usually  due  to  pyogenic  organ- 
isms— i.  e.,  suppuration  occurs. 
Proliferative  Periostitis. — ^This  is  a  proliferation  of  cells  of  the 
deeper  layers  of  the  periosteum  combined  with  emigrated  leuko- 
cytes.    A  node  is  thus  formed  which  may  ossify. 

Suppurative  Periostitis. — Pyogenic  organisms  may  enter  an 
injured  periosteum  or  one  weakened  by  previous  disease  (e.  g.,  by 
scarlet  fever).  The  origin  of  the  bacteria  is  byway  of  the  blood, 
either  directly  or  by  way  of  the  medulla  (as  a  secondary  effect  of  osteo- 
myelitis), or  by  way  of  the  skin. 

Pus  forms  beneath  the  periosteum,  raises  it,  and  destroys  its 
connection  with  the  bone.  The  vessels  are  stretched,  damaged,  and 
thrombosis  occurs.  Superficial  necrosis  of  bone  results,  which  may  be 
total  if  other  sources  of  blood  supply  are  also  cut  off". 


Absorption  of  blood  clot.  Section  through  the 
margin  of  a  clot  formed  among  the  tissues  by 
extravasation,  showing  the  growth  of  granula- 
tions by  which  it  is  removed:  a  a,  portions  of 
clot;  hh,  original  tissue;  cc,  granulations  spring- 
ing from  the  original  tissue  and  projecting  into 
the  clot;  dd,  wandering  cells  or  leukocytes  that 
seem  to  have  taken  red  blood  disks  into  their 
interior.  (Section  cut  in  gum  arable  and  stained 
with  hematoxylin.)      X  350.     (Black.) 


1  Schmau.s  and  Ewing,  Pathology  and  Pathological  Anatomy. 


INFLAMMATION  OF  BONE 


135 


Fio.  71 


Acute  Osteomyelitis. — This  is  a  suppuration  occurring  in  the  bone- 
marrow,  which  infects  the  bone  proper,  causes  much  thrombosis  of 
vessels,  coagulation  necrosis  of  bone  cells,  and  may  rapidly  cause  much 
necrosis  of  medullary  tissue.  Occurring  in  large  bones,  much  toxin  is 
produced,  which  may  rapidly  cause 
death.  The  organisms  and  thrombi 
formed,  becoming  emboli,  may  rap- 
idly lead  to  pyemia.^  Prompt  sur- 
gical interference  is  called  for. 

Inflammation  of  bone  may  lead  to 
its  rarefaction  (rarefying  osteitis  or 
osteoporosis),  its  condensation  (con- 
densing osteitis  or  osteosclerosis), 
or  its  death  (necrosis  and  caries). 

Rarefying  Osteitis  (Osteoporosis).— In  the  rarefying  process 
which  occurs  in  chronic  inflammation,  granulation  tissue  is  formed, 
which  enters  the  Haversian  canals  and  spaces  of  spongy  bone  and 


-y 


Trabeculae  of  bone  with  pcrforatins 
canals.      X  50. 


Fig.  72 


Fig.  73 


^—c 


^)  •- 


Z**"* 

o}^ 


-a 


// 


Section  of  bone  and  periosteum  covering  it:  B, 
bone;  c,  outer  fibrous  layer;  a,  inner  layer  of 
white  fibrous  tissue;  O,  layer  of  osteoblasts,  some 
of  which  reach  the  bone  with  their  prolongations. 
(Black.) 


Section  of  bone  and  periosteum  cover- 
ing it:  a,  osteoclasts,  cells  that  absorb 
bone;  6,  surface  of  bone,  showing  fibers 
of  periosteum  penetrating  it  and  a  How- 
ship  lacuna.     (Black.) 


destroys  (resorbs)  the  bone.  They  thus  form  new  channels  between 
the  spaces — perforating  canal  resorption  (Fig-  71).  With  suppuration 
(ulceration)  added,  the  granulations  break  down,  leaving  the  bone  as  a 
dead,  spongy,  or  honeycombed  mass.     This  is  caries  of  bone.     In  the 


'  Park's  Surgery. 


136 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM 


early  stages  the  inflammation  may  cease,  and  the  bone  not  only  be 
restored,  but  condensed. 

Condensing  Osteitis  (Osteosclerosis). — In  chronic  inflammation, 
instead  of  rarefaction,  the  trabeculae  of  bone  may  increase  in  thickness, 
so  that  all  spaces  and  Haversian  canals  become  smaller.  The  bone 
becomes  very  compact,  and  if  built  up  in  excess  of  its  orginal  dimen- 
sions, constitutes  the  condition  known  as  exostosis.  Both  condensing 
and  rarefying  osteitis  occur  about 
the  alveolar  process  and  the  roots  of 
teeth.  (See  Hypercementosis  and 
Resorption.) 

Necrosis  of  Bone. — Necrosis  of 
bone  following  rarefying  osteitis  is 
known  as  caries.  It  is  a  molec- 
ular death  of  bone.      Subperiosteal 


Fig.  74 


I/attioe-work  figures  in  halisteresis. 
V.  Recklinghausen.) 


(After 


mfMm 

^'^■ 

Diagram  of  healing  fracture.  From 
a  guinea-pig  ten  days  after  injury: 
K,  ends  of  the  bone;  m,  marrow;  c, 
periosteal  callus;  d,  medullary  callus; 
o,  osteoid  tissue.      X  6. 


death  of  l)onc  occurs  from  infective  periostitis,  and  is  due  to  the  com- 
pression of  vessels  by  the  exudation  and  to  thrombosis.  Nutrition 
ceases;  death  results.  The  dead  piece  is  demarked  by  a  line  of  leuko- 
cytes (phagocytes),  solution  of  continuity  occurs  at  the  line  of  union 
with  the  living  bone,  and  the  piece  is  thrown  out  as  a  sequestrum. 
The  solution  is  effected  by  granulation  tissue  as  the  rarefying  process 
above  cited.      (See  Gangrene.) 

Resorption  of  Bone. — Under  conditions  of  chronic  inflammation 
bone  is  often  removed  l)y  neighboring  tissue  in  one  of  several  ways. 

Lacunar  Resorption. — In  this  form  the  bone  is  excavated  by  giant 
cells  into  bays  called  Howship's  lacuna?,  which  may  enlarge,  or  later 
a  reconstructive  action  may  occur  an<l  osteoblasts  may  fill  up  the  bays 
with  bone. 


FEVER 


137 


Perforating  Canal  Resorption. — This  has  l)cen  described  under 
Caries  of  Bone.  The  eanals  connecting  me(hdhiry  spaces  are  enlarged 
by  the  grannhition  tissue  formed  in  them  (Fig.  71). 

Halisteresis  Ossium. — In  this  form  of  resorption  the  bone  first 
undergoes  decalcification  and  the  matrix  is  later  removed  (Fig.  74). 
It  occurs  in  conditions  of   osteomalacia  as   in  pregnancy,  senility, 


Fig.  76 


•1 


The  same  preparation:  .V,  myelogenous  callus;  P,  periosteal  callus;  K,  ends  of  the  bone; 
k,  osteoid  trabeculie;  o,  osteoblasts  in  rows;  p,  thickened  periosteum.  X250.  (Schmaus 
and  Ewing.) 

etc.  It  also  occurs  in  the  alveolar  process,  and  is,  at  least  in  part, 
the  cause  of  the  cleanly  symmetrical  resorption  of  the  gum  and 
alveolar  margins  (Talbot).^ 

Regeneration  of  Bone. — Bone  lost  by  suppuration  is  first  replaced 
by  provisional  tissue  of  tiie  connective-tissue  type  in  which  appear 
osteoblasts.  Calcification  then  proceeds  under  superintendence  of 
these  (Figs.  75  and  76). 

FEVER. 

The  term  fever  is  applied  to  a  condition  the  most  prominent  feature 
of  which  is  an  elevation  of  the  bodily  temperature  above  the  normal, 
37°  C  To  constitute  a  fever  this  rise  in  temperature  must  continue 
for  some  leuirth  of  time. 


Interstitial  gingivitis. 


138  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

Causes. — ^Fevers  are  commonly  caused  by  the  presence  in  the  circu- 
latory fluids  of  substances  which  act  as  poisons  upon,  probably,  the 
nerve  centres  controlling  heat  production.  As  a  rule,  the  offending 
substance  is  a  poison  generated  in  the  body  through  the  action  of 
microorganisms.  The  character  and  type  of  the  fever  are  determined 
by  the  nature  of  the  offending  substances — i.  e.,  the  variety  of  infection. 

Classes. — Fevers  are  divided  into  periodical  or  continued,  according 
as  to  whether  there  is  a  periodical  fall  of  temperature  and  a  subsequent 
rise,  or  whether  the  fever  continues  practically  unabated  from  the  begin- 
ning to  the  termination  of  a  disease.  Fevers  are  classed  in  severity 
according  to  the  maximum  temperature,  and,  again,  according  to  their 
duration.  A  temperature  of  100.5°  to  101.3°  F.  is  called  slightly  febrile; 
101.3°  to  103°  F.  moderate  fever;  103°  to  105°  F.  marked  fever.  A 
temperature  above  106°  F.  is  termed  hyperpyrexia. 

Symptoms. — The  most  characteristic  symptom  of  fever  is  the  eleva- 
tion of  temperature;  accompanying  this  there  is  an  increased  frequency 
of  the  pulse.  In  acute  inflammatory  diseases  the  pulse  is  full  and 
bounding,  the  eyes  injected,  the  bowels  constipated,  and  the  urine 
scanty,  containing  an  excess  of  urea.  On  standing,  the  urine  throws 
down  a  brickdust  deposit  (urates).  In  fevers  of  a  lower  type,  or  in 
many  fevers  which  begin  as  described,  the  high,  bounding  pulse  is 
succeeded  by  a  soft,  quick  pulse,  and  evidences  of  great  debility.  In 
fevers  in  which  the  temperature  runs  high  there  is  commonly  evidence 
of  intoxication,  more  or  less  delirium,  and  reflex  muscular  action. 
With  a  persistent  temperature  and  a  pulse  becoming  softer  and  more 
frequent,  there  is  increasing  debility. 

Pathology  and  Morbid  Anatomy. — In  all  cases  of  continued  high 
temperature  the  fat  of  the  body  rapidly  disappears  and  granular  degen- 
eration occurs  in  the  muscles  and  viscera  of  the  body.  If  the  fever  be 
long  continued  and  of  an  adynamic  type,  this  degeneration  may  become 
marked.  Its  occurrence  in  the  muscles  of  the  heart  is  common  and  is 
an  element  of  danger.  There  are  an  increase  in  the  amount  of  carbon 
dioxide  formed  and  exhaled  from  the  body,  and  an  increased  amount  of 
oxygen  inhaled.  This,  with  the  increase  of  urea,  the  product  of  the 
oxidation  of  nitrogenous  tissues  (muscles,  glands,  etc.),  indicates  that 
the  oxidation  of  the  tissues  is  largely  increased;  hence,  the  elevation 
of  temperature.  As  repair  does  .not  equal  waste  in  fevers,  the  nutri- 
tive processes  being  profoundly  distur})e(l,  the  essential  elements  of  the 
tissues  suffer  from  the  increased  oxidation  and  undergo  degenerative 
changes. 


TOXEMIA  139 

Prognosis. — The  higher  the  temperature  and  the  longer  it  continues, 
the  greater  drain  there  is  upon  the  vital  forces.  As  a  rule,  a  tempera- 
ture of  106°  F.  persisting  more  than  twenty-four  hours  presages  death. 
If  the  vital  forces  flag  and  the  heart  action  becomes  weakenerl,  and  if 
there  be  evidence  of  profound  intoxication,  such  as  twitching  of  ten- 
dons, low,  muttering  delirium,  and  a  clammy  surface,  the  outlook  is 
bad.  Favorable  signs  are  falling  temperature,  a  clear  eye,  tongue 
losing  its  coating,  free  action  of  the  bowels,  free  perspiration,  free 
action  of  the  kidneys,  and  a  good  vascular  tension. 

Treatment. — In  the  light  of  present  knowledge,  efforts  should  first 
be  made  to  discover  the  nature  of  the  cause  of  the  fever  and  to  remove 
it,  if  possible.  If  not,  attention  shoidd  be  directed  to  maintaining  the 
vital  forces  until  the  body  rids  itself  of  the  offending  causes.  As  many 
fevers  are  self-limited  in  course  and  duration,  this  latter  treatment 
becomes  an  important  consideration.  The  temperature  should  be 
kept  within  safe  limits  by  the  administration  of  antipyretics,  when  the 
condition  of  the  heart  will  permit  their  use,  and  also  by  cool  sponging 
or  cool  baths.  The  action  of  the  lieart  shoidd  be  sustained  by  the 
administration  of  concentrated  nutriment,  and  by  stimulants  when 
necessary.     The  bowels  must  be  kept  open. 

In  any  form  of  fever  there  is  no  therapeutic  measure  comparable 
with  the  removal  of  the  cause,  provided  this  be  discoverable,  identified 
and  removable. 

TOXEMIA. 

By  toxemia  is  meant  a  more  or  less  general  disturbance  of  the 
economy  as  the  result  of  the  presence  in  the  blood  of  substances 
poisonous  to  a  tissue  or  the  tissues.  The  substance  may  be  a  normal 
constituent  of  the  blood  which  has  accumulated  owing  to  faulty 
elimination — e.g.,  urea — or  be  derived  from  the  alimentary  canal  as 
the  result  of  unusual  fermentation  therein.  Such  an  effect  is  known 
as  auto-intoxication.  It  may  be  due  to  the  action  of  drugs  of  toxic 
character — e.  g.,  alcohol  or  iodoform.  This  is  drug  toxemia.  Again, 
it  may  be  due  to  the  action  of  the  products  of  bacteria,  which  products, 
absorbed  from  certain  foci  of  infection,  produce  general  eft'ects,  such 
as  fever.  Again,  similar  results  can  be  produced  by  the  introduction 
of  toxic  products  from  bacterial  culture  in  vitro  or  in  experimental 
animals. 

Septic  Intoxication. — By  septic  intoxication  is  meant  the  absorption 
into  the  blood  of  the  products  of  bacterial  activity,  which  products  are 


140  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

produced  at  some  focus  or  foci  of  infection  as  the  result  of  tissue  or 
tissue-juice  decomposition.  These  bacterial  products  produce  symp- 
toms of  general  poisoning  or  intoxication,  which  are  mild  or  severe, 
according  to  the  character  of  the  poisonous  body  produced-  The 
organisms  do  not  necessarily  enter  the  blood,  hence  the  blood  is 
not  infectious  if  inoculated  into  another  person  (or  experimental 
animal). 

Two  varieties  of  septic  intoxication  may  be  distinguished: 

1.  Intoxication  by  the  products  of  the  action  of  specific  bacteria 
developing  upon  living  tissue. 

2.  Intoxication  by  the  action  of  bacteria  upon  non-vital  materials 
(sapremia). 

The  action  of  the  bacilli  of  diphtheria,  Asiatic  cholera,  and  tetanus 
are  examples  of  the  first  class.  Their  toxins  are  virulent,  but  the 
bacteria  are  confined  to  the  pharynx,  intestine,  and  the  wound, 
respectively. 

Sapremia. — The  entrance  of  putrefactive  or  the  pyogenic  organ- 
isms into  such  material  as  a  large  blood  clot  or  gangrenous  area  may, 
by  putrefaction,  cause  the  formation  of  large  quantities  of  toxins. 
These,  if  absorbed,  produce  rapid  and  profound  symptoms  of  intoxi- 
cation. The  symptoms  vary  according  to  the  nature  of  the  toxin  and 
the  quantity  absorbed,  but  ordinarily  occur  in  the  following  order: 
malaise,  rigor,  fever  and  its  symptoms,  nausea,  vomiting,  headache, 
diarrhea,  prostration,  delirium  in  some  cases,  muscular  weakness, 
clammy  skin,  feeble  pulse,  quick  respiration,  and  in  fatal  cases  coma 
and  death.  The  symptoms  are  similar  to  those  of  septicemia,  but 
appear  more  rapidly — i.  e.,  septicemia  requires  time  to  spread.  There 
is  a  putrid  wound  which  is  the  source  of  the  toxic  substance.  The 
condition  is  usually  complicated  by  septicemia. 


SEPTICEMIA   (GENERAL  SEPTIC  INFECTION). 

By  septicemia  is  meant  a  condition  in  which  the  bacteria,  usually 
one  of  the  pyogenic  varieties,  gain  entrance  to  the  living  tissues,  enter 
the  circulation,  and  are  carried  to  inaccessible  parts,  where  their 
development  continues  and  from  which  point  their  toxins  are 
absorbed  (Fig.  77). 

This  process  requiring  more  time  than  mere  absorption  of  toxins, 
the  symptoms  are  much  more  delayed  than  in  sapremia.     The  blood 


SEPTICEMIA  141 

is  highly  infective  to  susceptible  animals  in  minute  amount,  as  it 
contains  bacteria. 

Pathology. — There  is  a  septic  wound  in  which  incubation  occurs  for 
several  days.  The  lymphatics  lea(Mng  from  the  part  and  the  nearest 
lymphatic  glands  become  inflamed.  In  pronounced  cases  the  spleen 
is  enlarged.     There  is  marked  leukocytosis. 

Examination  made  after  death  from  the  septic  intoxication  pro- 
duced by  both  sapremia  and  septicemia  exhibits  fairly  constantly 


a 


^. 


a 
b 


%^ 

-A                                                     > 

^>  . 

-J                  ^' 

r  ^ 

\     <:^  V 

r 

./ 

a 


Pectoral  muscle  beset  witli  large  numbers  of  the  Streptococcus  pyogenes,  from  a  case  of 
phlegmonous  inflammation  of  the  subcutaneous  and  intermuscular  connective  tissue,  due  to 
cadaveric  poisoning  (the  phlegmon  of  the  wall  of  the  chest  developed  two  days  after  the 
finger  was  injured,  and  the  intermediate  lymph  vessels  of  the  arm  showed  no  evidences  of  being 
involved):  a,  perimysium  internum  full  of  streptococci;  b,  transversely  cut  muscular  fibers, 
still  intact;  r,  transversely  cut  muscular  fibers  wliich  are  beginning  to  degenerate;  d,  muscular 
fibers  into  which  the  cocci  have  penetrated.  (Preparation  treated  with  gentian  violet  and 
vesuvin,  and  mounted  in  Canada  balsam.      X  350  diameters.)     (Ziegler.) 

enlargement  of  the  spleen  and  disintegration  of  the  red  corpuscles, 
with  staining  of  the  intima  of  the  vessels  and  heart.  The  lungs  are 
congested.     Death  occurs  through  heart  failure.^ 

Symptoms. — These  are  similar  to  those  of  sapremia,  except  that  the 
periods  of  incubation  about  the  body  cause  delays. 

Treatment. — For  sapremia  and  septicemia,  the  treatment  is  both 
local  and  general.  The  local  treatment  involves  the  opening  and  dis- 
infection of  all  wounds,  even  the  extirpation  of  a  part  and  of  neighbor- 
ing glands  being  sometimes  necessary  for  removal  of  the  cause.     If 

'  Green,  Pathology  and  Morbid  Anatomy. 


142  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

possible,  the  part  is  immersed  frequently  in  hot  water,  which  may 
occasionally  have  mercuric  chloride  added  to  it. 

An  antiseptic  salve,  consisting  of  resorcin,  5  parts;  ichthyol,  10  parts; 
unguentum  hydrargyri,  40  parts;  lanolin,  45  parts,  is  to  be  applied  to 
the  area  of  infection.^ 

Crede's  silver  ointment  may  be  applied  to  the  unbroken  skin  for 
the  systemic  antiseptic  effect  of  the  silver. 

The  general  treatment  consists  in:  (1)  Clearing  the  alimentary 
canal  by  means  of  cathartics  and  maintaining  its  asepsis  by  means  of 
mercuric  chloride  in  small  doses,  salol,  or  other  suitable  antiseptic. 

(2)  Supporting  the  heart  action  by  means  of  alcohol  and  strychnine. 

(3)  Supporting  the  strength  by  concentrated  liquid  nourishment,  such 
as  egg  albumen,  beef  peptonoids,  beef  juice,  peptonized  milk,^  to 
which  diet  fruit  may  be  added.^  (4)  Reducing  the  temperature  by 
means  of  cold  sponge  baths  or  quinine.  (5)  Maintaining  the  elimina- 
tive  action  of  the  kidneys  until  the  system  has  rid  itself  of  the  toxins. 
For  the  more  profound  cases  Park  recommends  hte  intravenous 
infusion,  as  an  intravascular  germicide,  of  from  500  c.c.  to  1000  cc. 
of  a  solution  of  Credd's  soluble  silver,  1  to  1000  of  sterilized  water  at 
105°  F.     Streptococcus  antitoxin  is  of  value. 


PYEMIA. 

By  pyemia  is  meant  a  form  of  septicemia  or  septic  infection  by 
pyogenic  organisms,  which,  locating  at  favorable  spots,  as  in  the 
capillaries,  multiply  and  produce  numerous  abscesses  known  as 
miliary  or  metastatic  abscesses.  From  these  foci  toxins  are  absorbed, 
which  produce  a  septic  intoxication. 

The  organisms  may  enter  the  blood  from  some  focus  of  suppuration 
as  free  cells  or  be  taken  up  by  leukocytes,  or  thrombosis  may  occur  at 
the  original  focus  of  infection  and  portions  of  clot  be  carried  in  the 
blood  as  septic  emboli  to  terminal  arteries,  where  the  results  of  septic 
infarction  are  set  up.      (See  Infarction.) 

Symptoms. — ^^Fhe  symptoms  of  pyemia  are,  in  general,  those  of 
septicemia;  their  appearance  is  delayed  from  the  date  of  the  reception 
of  an  injury  or  the  outbreak  of  the  primary  suppuration.  The  onset 
of  pyemia  is  usually  by  a  chill  or  a  succession  of  chills.     Each  fresh 

1  Park's  Surgery. 

2  Thompson's  Practical  Medicine. 
'  Parlf's  Surgery. 


THE  EXANTHEMATA  143 

area  of  pus  formation  is  believed  to  be  announced  by  a  chill  and  a  rise 
of  temperature.  The  temperature  is  subject  to  remissions,  and  sudden 
variations  in  its  height  are  noted.  The  general  symptoms  are  those 
of  an  adynamic  fever.  Local  symptoms  appear  according  to  the  point 
of  lodgement  of  septic  emboli.  Pus  centres  may  be  found  in  the  lungs, 
and  cause  symptoms  of  dyspnea;  collections  frequently  occur  in  joints, 
causing  loss  of  mobility;  eruptions  appear  on  the  skin,  the  swellings 
being  apparent;  typhoid  symptoms  become  more  pronounced,  and  an 
increasing  debility  ushers  in  a  usually  fatal  ending.  At  times  both 
septicemia  and  pyemia  may  become  chronic. 

Treatment. — The  treatment  of  pyemia  should  be  preventive.  The 
carrying  out  of  rigid  antiseptic  precautions  has  much  lessened  the 
frequency  of  pyemia.  If  areas  of  infection  are  removable,  they  are 
removed  no  matter  what  extent  of  operation  may  be  necessary.  The 
general  treatment  is  the  same  as  in  septicemia,  with  much  less  hope 
of  recovery. 

A  consideration  of  the  infective  surgical  processes  in  connection  with 
dental  and  oral  diseases  is  of  the  utmost  moment  to  the  practitioner  of 
dentistry.  Nearly  all  of  the  diseases  which  the  dentist  is  called  upon 
to  treat  are  infective  from  their  inception.  Moreover,  the  saliva,  hold- 
ing in  suspension  numerous  forms  of  bacteria,  both  saprophytic  and 
parasitic,  and  their  waste,  is  a  highly  infective  fluid. 

It  has  been  clearly  demonstrated  by  the  researches  of  INIiller*  that 
many  forms  of  bacteria  found  in  specific  diseases,  and  found  inhabiting 
the  intestinal  tract,  are  more  or  less  constantly  present  in  the  human 
mouth,  and  that  the  pathway  in  many  general  infections  is  no  doubt 
via  the  oral  cavity.  A  wound  made  in  the  human  mouth  is  necessarily 
an  infected  wound.  In  the  vast  majority  of  cases  the  body  exercises 
its  protective  function  in  a  phagocytosis,^  or  through  immunizing 
processes,  which  disposes  of  invading  bacteria  or  renders  them 
innocuous.  In  other  cases  it  is  beyond  question  that  this  protective 
provision  fails  and  infection  occurs,  especially  if  new  forms  be 
introduced.     The  saliva  is  not  germicidal  in  any  way  (iNIiller). 

THE  EXANTHEMATA. 

Certain  acute  specific  diseases,  such  as  rubeola,  rotheln,  scarlatina, 
varicella,  and  variola   are  accompanied  by  skin  eruptions  generally 

•  Microorganisms  of  the  Human  Mouth. 
'  Hugenschmidt,  Dental  Cosmos,  1896. 


144  DISTURBANCES  OF  THE  VASCULAR  SYSTEM 

distributed  over  the  body,  and  which  represent  an  infective  dermatitis ; 
indeed,  the  ei-uptions  of  many  of  these  diseases  are  contagious  to 
other  individuals.  Syphihs,  a  chronic  specific  disease,  produces 
similar  effects. 

The  special  interest  lying  in  the  exanthemata  is  that  occurring  dur- 
ing the  development  of  the  teeth;  the  latter  are  often  profoundly  affected 
so  that  malformations,  sometimes  serious  in  character,  occur  in  the 
teeth.  It  is  to  be  recalled  that  teeth  are  dermoid  structures,  certainly 
in  so  far  as  the  enamel  is  concerned.  (See  Malformations  of  the  Teeth.) 
Again,  after  or  during  exanthematous  diseases,  notably  scarlet  fever, 
the  oral  tissues  are  much  debilitated,  so  that  abscesses  about  the  teeth 
may  produce  much  necrotic  tissue. 


SECTION  II. 

EMBRYOLOGY,  ANATO^IY,  AND  HISTOLOGY. 


CHAPTER    VI. 

THE  DEVELOPMENT,  ANATOMY,  AND  HISTOLOGY  OF  THE 
JAWS  AND  TEETH. 

As  malformations  of  the  parts  about  the  mouth  and  of  the  teeth  are 
dependent  upon  defective  development  of  the  same,  it  is  incumbent 
that   certain    facts    concerning 

their    embryology    should     be  ^^°-  "^^ 

stated.  In  like  manner,  as  the 
processes  of  pathology  are  modi- 
fi(Hl  by  the  peculiar  anatomy  of 
the  teeth  and  associated  parts, 
it  is  necessary  that  a  previous 
knowledge  of  these  be  acquired 

before  the  special  dental  path-        f^s^-  x — ^       ^)  M  jyj 

ology   can    be    comprehended.      'O^^p-  \S-J^^ /mS^ ^^^ml^ 

The   embryology  of   the  mouth      s^;^—:  '^"''f'JKi^^m   4 

begins  at  a  very  early  period —      4^^^R_       ^       .mIIII  -^^^  6 
before  the  twelfth  day  the  future 
mouth    may    be  located   (His,         ^ 
Fig.     78).      The    mouth    and    ,       "gM-"-©^- 
nasal  cavity  are  circumscribed 
by  parts  which  are  developed  by 

outgrowths   from   the   head    fold  ^'■•''■^"^  >»"  ^'"'"•y"  °f  twenty-five  to  twenty- 

°  eight  days  (magnified  fifteen  times):   1,  frontal 

of    the  fetus.       Those   structures  prommence;   2,  3.  right  antl  left  olfactory  fossa; 

]•    ,    1                               ]               j.l,„  4,   inferior    maxillary    tubercles,   united    in    the 

immediately  concerned  are  the     ^j^j^,,^  ,5^^.  5  ^^,,^,.^,^  maxillary  tubercles;  6. 

lateral     tubercles    arising     from      n""i»l»   or  fauces;    7,   second   pharyngeal   arch: 
.  ,S.  third;  9,  fourth;   10.  primitive  ocular  vesicle; 

the     frontal      prominence      (rig.       n,  primitive  auditory  vesicle.     (Gray.) 

79),  which  grow  downward  and 

fuse,  forming  the  nose,  the  nasal  septum,  the  intermaxillary  bones, 
and  anterior  portion  of  the  upper  lip  (Figs-  80  and  81).     From  the 
10 


146     AX  ATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AND   TEETH 


sides  of  the  head  fold  at  the  level  of  the  mouth  and  neck  appear 
certain  lateral  protuberances,  or  pharyngeal  arches.  The  first 
pharyngeal  arches    (Fig.  78,  4)    divide  into    (1)   the  superior  max- 


FiG.   79 


Sup.  tubercle 
Lateral  tubercle 


Sup.  tubercle 
Lateral  tubercle 


Head  of  an  early  human  embryo,  showing  the  disposition  of  the  facial  fissures  and  the 
superior  and  lateral  tubercles.     (His.) 


S.M.P; 


S.M.P. 


I.M. 


NAS. 
Diagram  illustrating  scheme  of  union  of  the  processes;     NAS.,  lateral  tubercles  forming  in- 
ternal maxillary  Vjones,  INT.  MAX.,  and  nasal  septum;   S.M.P.,  superior  maxillary  processes 
forming  palatal  proces.ses  of  superior  maxilla;,  S.M.P.;   N.C.,  nasal  cavity;   O.C,  oral  cavity; 
I.M.,  inferior  maxillary  processes  united. 

illary  processes  (Fig.  78,5)  and  (2)  the  inferior  maxillary  processes 
(P'ig.  78, 4,  shown  just  beneath  the  oral  cavity  and  united  in  the  median 
line). 


ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH     I47 

Fig.   81 


Complete  bilateral  fissures  (coloboma)  of  face.     (Guersant.) 

Tir,.  <?2 


Vertical  transverse  section  through  head  of  himian  embryo,  about  the  tenth  week:  1,  na.sai 
cartilage;  2,  buccal  cavity;  3,  tongue;  4,  dental  ridge,  lower  jaw;  .5,  nasal  cavity;  6,  dental  ridge, 
upper  jaw;  7,  dental  ridge,  lower  jaw.      X  30.     (Broomell.') 

'  Anatomy  and  Histology  of  the  Mouth  and  Teeth. 


148      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

The  superior  maxillary  processes  develop  the  palate  bones  and  the 
superior  maxillae.  They  form  the  balance  of  the  upper  lip.  The 
arch  itself  forms  the  cheek.  Fig.  81,  from  a  case  of  arrested  develop- 
ment, illustrates  the  unions  and  parts  naturally  formed,  but  here 
incomplete. 

Secondary  processes  develop  horizontally  toward  each  other  form 
the  palatal  portions  of  the  superior  maxillse  and  palate  bones  and 
unite  at  the  median  line  (Fig.  80,  S.M.P.,  also  Fig.  81),  forming  the 
vault  of  the  mouth  and  floor  of  the  nasal  cavity.  Union  occurs  with 
the  lateral  processes,  later  forming  the  intermaxillary  bones  and  bear- 


FiG.  83 


One  for  nasal  and 
facial  portions. 


One  for  orbital  and 
malar  por lions. 


One  for  incisive 
portion. 


One  for  palatal 
portion. 


Alder  lor  Surface. 


At  birth. 


Inferior  Surface. 

Development  of  the  superior  maxillary  bone  by  four  centres;  also  development  of 
intermaxillary  bones.     (Gray.') 

ing  the  germs  of  the  incisor  teeth  (Fig.  83),  thus  completing  the 
formation  of  the  upper  jaw  and  lip. 

The  inferior  maxillary  processes  grow  forward  and  unite  at  the 
median  line,  developing  the  inferior  jaw  and  lip. 

The  structures  of  the  floor  of  the  mouth  and  neighboring  structures 
are  formed  from  the  second,  third,  and  fourth  pharyngeal  arches  and 
a  tubercle  arising  near  the  first  pharyngeal  arch.  The  fusions  of  the 
lateral  portions  of  the  upper  maxilla?  begin  first  anteriorly  at  about  the 
eighth  week  and  progress  posteriorly  until  complete  at  about  the 
eleventh.  Malformations  due  to  non-union,  therefore,  date  from  this 
period,  and  consist  of  the  following  typical  varieties: 


'  Gray's  Anatomy. 


ANATOMY   AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH     149 


1.  Non-union  of  lip  on  one  or  botli  sides — simple  harelip. 

2.  Non-union  of  lip  and  of  maxilla  and  intermaxillary  bone  on  one 
side  (harelip,  Figs.  84  and  85). 


Fig.  84 


Fig.  85 


Cleft  of  liard  and  soft  palate:  rudimentary 
intermaxillary  bone  placed  in  advance  of  lips. 
(Mason.) 

Fig.  86 


Cleft  of  hard  and  soft  palate. 
(Mason.) 


Median  fissure  of  the  lower  lip  and  chin.     (Marshall,  after  Wofler.) 

3.  Non-union  of  lip  and  intermaxillarv  hone  on  both  sides  (double 
harelip,  Fig.  81). 

4.  Non-union  of  all  horizontal  processes  in  the  median  line  (cleft 
palate,  Figs.  84  and  85). 

5.  Non-union  of  halves  of  soft  palate  (cleft  velum). 

6.  Non-union  of  halves  of  the  uvula  (bifid  or  cleft  uvula). 


150     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

Combinations  of  cleft  velum  and  cleft  palate  or  of  cleft  palate  and 
single  or  double  harelip  may  exist. 

Fig.  81  shows  the  parts  in  their  ununited  state. 

The  failure  of  the  inferior  maxillary  processes  to  unite  is  rare,  but 
is  occasionally  seen  (Fig.  86).  The  inferior  maxillary  tubercles 
develop  a  transitory  support  to  the  lower  jaw  known  as  Meckel's 
cartilage.  The  cartilages  of  the  right  and  left  side  do  not  fuse 
together  at  the  future  symphysis  (Hertwig) .     (Fig.  87.) 

It  acts  as  a  support  to  the  fetal  jaw,  undergoes  atrophy  at  about  the 
sixth  month  of  gestation,  and  at  birth  but  few  fragments  are  found 
near  the  symphysis.  At  birth  ossification  has  occurred,  and  the  bone 
consists  of  two  halves  united  by  a  fibrous  symphysis  in  which  ossifi- 
cation takes  place  during  the  first  year  (Gray). 


Fig.  87 


Fig.  88 


M.C. 


Showing  Meckel's  cartilage  (MC)  in  longi- 
tudinal and  transverse  section. 


Osteology  of  harelip.      (Museum  of  the 
Philadelphia  Dental  College.) 


A  case  of  failure  of  development  of  the  intermaxillary  bones  has 
been  reported,^  the  space  between  the  cuspid  teeth  being  about 
one-eighth  inch. 

The  end  of  the  cartilage  in  the  base  of  the  inferior  maxillary  process 
becomes  the  future  malleus  (one  of  the  bones  of  the  middle  ear).  The 
portion  of  the  cartilage  running  from  the  malleus  to  the  formed  bony 
lower  jaw  becomes  transformed  into  the  internal  lateral  ligament  of 
the  inferior  maxilla  (Hertwig). 

It  is  to  be  remembered  that  these  processes  are  formed  by  the  out- 
growth of  the  mesotjlastic  layer  of  the  })lastoderm  and  are  covered  by 


»  Jeffery,  British  Dental  Journal,  July,  1904. 


DEVELOPMENT  OF  THE  TEETH  151 

epithelial  tissue  springing  from  the  epiblast.  Both  are  concernefl  in 
the  formation  of  the  teeth.  Epithelium  is  reflected  over  the  face  and 
oral  cavity. 

DEVELOPMENT  OF  THE  TEETH. 

At  about  the  sixth  week  of  gestation,  while  the  maxillary  processes 
are  but  ill-defined  masses  of  mesoblastic  tissue  surrounded  on  all 
sides  by  epiblastic  tissue  (Fig.  82),  the  "dental  band"  develops  as  a 
continuous  depression  of  the  stratum  ]\Ialpighii  of  the  mucous  mem- 
brane extending  from  end  to  end  of  the  fetal  jaw,  over  which  depres- 

FiG.  89 


Porcine  embryo:  ep,  epithelium,  infant  layer  or  stratum  Malpighii;  cl,  embryonal  connective 
tissue  witli  large  intercellular  interspaces.      1)^   cm.  X  250.     (Sudduth.) 

sion  is  a  mound  of  epithelial  cells  developed  from  it  and  called  the 
"dental  ridge"  (maxillary  rampart  of  KoUiker  and  Waldeyer,  Fig. 
90,  6,  and  Fig.  91,  &). 

At  ten  points  on  the.se  bands  in  each  jaw,  at  about  the  seventh  to 
theeighth  week,  a  further  depression  of  the  stratum  Malpighii  occurs, 
of  a  more  or  less  definite  saccular  form,  the  sac  also  containing  embry- 
onic epithelial  colls  (Figs.  91 ,  c,  and  92, 3).  This  enlarges  by  an  interior- 
ward  growth  of  epithelial  cells,  while  the  attachment  to  the  mucous 
membrane  remains  constricted.  At  the  ninth  week  the  mesoblastic 
tissue  beneath  has  somewhat  condensed,  evidencing  the  first  appear- 
ance of  the  dentinal  papilla.  At  this  .stage  the  .sac  (enamel  organ)  has 
been  likened  in  appearance  to  a  Florentine  flask  (Fig.  93,  2).  The 
dentinal  papilla  pushes  up  the  base  of  the  enamel  organ,  which  grad- 
ually adapts  itself  over  the  papilla,  assuming  finally  a  saddle  shape 
(Figs.  94  and  95). 


152     ANATOMY   AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

At  the  sixteenth  week  the  enamel  organ  has  developed  so  as  to 

contain  three  distinct  formative  parts  concerned  in  enamel  deposition. 

1.  Next  to  the  papilla  the  cells  of  the  stratum  Malpighii  develop 


Fig.  90 


\o.t- 


u 


ct 


Longitudinal  transverse  section  of  the  infeiiur  maxilla  of  a  porcine  embryo:  fc,  band,  solid  at 
.anterior  portion,  but  divided  posteriorly  into  band  and  lamina.     3  cm.  X  40.     (Suddutli.) 


Fig.  9] 


Vertical  section  through  band  from  jaw  of  porcine  embryo:  e-p,  epithelium;  b,  band;  r,  cord; 
rf,  connective  ti.nsue.     'iVi  cm.     X  60.     (Sudduth.) 


DEVELOPMENT  OF  THE  TEETH 


153 


into  nucleated  columnar  cells;  the  ameloblasts,  the  office  of  which  is  to 
deposit  enamel  (Fig.  96,  c  d,  and  Fig.  97,  c). 

2.  Those  next  interior  develop  into  large  cells  nutritively  associated 
with  the  ameloblasts  and  collectively  called  the  stratum  intermedium 
(Fig.  97  6). 

3.  Those  in  the  central  portion  of  the  enamel  organ  are  large  cells 
rich  in  calcific  material  and  polygonal  from  mutual  pressure,  and 
called  collectively  the  stellate  reticulum.  They  furnish  the  first 
nutritive  material  for  the  enamel  cells  (Fig.  94,  1,  and  Fig.  96,  a). 

Fig.  92 


Section  of  jaw,  embryo  of  pig,  sfiownng  growth  of  enamel  organ:  1,  epithelium;  2,  stratum 
Malpighii;  3,  first  stage  in  growth  of  enamel  organ  of  temporary  tooth;  4,  embryonic  connec- 
tive tissue;  5,  aeveloping  bone  of  jaw.     (.Vndrews.) 

The  dentinal  papilla  develops  a  reticulum  of  blood ves.sels,  nerves, 
and  branched  stellate  connective-tissue  cells  lying  in  a  gelatinous 
matrix.  Upon  the  surface  of  the  papilla  elongated  nucleated  con- 
nective-tissue cells  called  odontoblasts  are  found,  the  office  of  which 
is  to  deposit  dentine  (Fig.  97,  e).  About  the  enamel  organ  and  den- 
tinal papilla  a  fibrous  sac  develops  from  the  mesoblastic  ti.ssue, 
encloses  them,  and  is  called  the  follicular  wall  (Fig.  95,  c.  ct.),  and  will 
become   the  pericementum  or   cementum   organ.     The   entire   wall 


154     ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

and  its  enclosures  are  called  the  dental  follicle  (Fig.  95).  At  the 
sixteenth  week  the  cord  of  the  temporary  enamel  organ  gives  off 
from  its  side  a  cord  which  will  form  the  enamel  organ  of  the  suc- 
ceeding permanent  tooth,  and  a  cord  is  given  off  from  the  mucous 
membrane  for  the  first  permanent  molar  (Fig.  95,  ep) .  At  the  seven- 
teenth week  dentine  deposition  begins  by  the  extrusion  of  small 
calcospherites  formed  within  the  odontoblasts,  composed  chemically 


Fig.  93 


Section  of  jaw,  embryo  of  pig,  showing  gwwth  of  enamel  organ:   1,  epithelium;  2,  second  stage 
in  growth  f)f  enamel  organ;    3,  embryonic  connective  tissue.      (Andrews.) 

of  calcium  and  magnesium  salts  combined  with  albumen,  and  known 
as  calcoglobulin.  These  calcospherites  are  evidently  piled  against  the 
ameloblasts  and  later  against  each  other,  and  around  protoplasmic  pro- 
longations of  some  of  theof]onto})lasts,  which  prolongations  remain  in 
similarly  compiled  tube-like  structures  known  as  tubule  walls  or  sheaths 
of  Neuman,  while  the  odontoblasts  themselves  recede,  finally  persist- 
ing upon  the  surface  of  the  pulp  (Figs.  97,  99,  105,  117,  US,).    After 


DEVELOPMENT  OF  THE  TEETH 


155 


some  dentine  has  been  deposited  enamel  deposition  begins.  The 
ameloblasts  in  hke  manner  form  within  themselves  calcospherites  or 
enamel  globules,  also  an  amorphous  substance  called  interprismatic 
cement  substance.  Both  are  calcoglobulin,  but  the  latter  contains 
less  organic  matter,  at  least  finally,  than  the  dentinal  calcoglobulin. 

The  ameloblast  first  extrudes  a  drop  of  interprismatic  cement 
substance  against  the  dentine,  and  into  it  deposits  an  enamel  globule 
(Williams).  This  is  repeated,  the  ameloblasts  meanwhile  receding, 
the  result  in  finished  enamel  being  a  rod  composed  of  enamel  globules 

Fig.  94 


Section  of  jaw,  cnilnyo  ol  jug,  slHiwmg  growth  of  enaiuel  organ  and  dentine  Kum:    1,  enamel 
oiKan;   2,  dentine  gum;    3,  growth  of  jaw;   4,  tongue.      (.\ndiews.) 

united  inarowbyintervein'nglayersof  interprismatic  cement  substance. 
The  scheme  of  formation  is  shown  in  Fig.  99,  and  the  orderly  arrange- 
ment in  Fig.  113.  The  hexagonal  arrangement  shown  in  transverse 
section  (Fig.  114,  B)  is  due  to  mutual  pressure  of  the  globules.  Each 
rod  is  united  laterally  to  its  neighbor  1)V  interprismatic  cement 
substance,  which  flows  there  during  deposition  of  each  layer  of  the 
enamel.  The  str'uv  of  the  enamel  represent  periods  of  incremental 
activity.  That  the  enamel  rod  is  not  formed  by  calcification  of  the 
ameloblast  is  proven  by  the  fact  that  the  ameloblast  lies  at  an  angle 


156     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

to  the  developing  rod.  The  ameloblasts  and  remains  of  the  enamel 
organ  persist  as  Nasmyth's  membrane,  a  structure  epithelial  in  char- 
acter, 5-^  in.  in  thickness  (Hopewell-Smith)  and  quite  resistant  to 


Fig.  95 


Vertical  trannverse  section  of  jaw  of  porcine  embryo,  injected:  ep,  epithelium,  with  (il)  infant 
layer;  a,  layer  of  ameloblasts;  o,  layer  of  odontoblasts;  cp,  cord  for  permanent  tooth;  ot,  outer 
tunic;  it,  inner  tunic;  ar,  stellate  reticulum;  7/)h  ep,  whorls  of  epithelium  forced  from  outer 
tunic  and  stellate  reticulum;  d,  dentine;  dp,  dentinal  pulp;  v,  bloodvessels  of  pulp;  ct,  connec- 
tive tissue;  c  cl,  follicular  wall;  p,  periosteum;  sp,  space.      10  cm.      X  00.     (Suddufh.) 

acids,  louring  the  deposition  of  enamel  and  dentine,  bone  is  formed  in 
islets  which  appear  in  the  mesoblastic  structure  between  the  follicle 
wall  and  the  periosteum  (Fig.  95).     These  gradually  coalesce  until 


DEVELOPMENT  OF  THE  TEETH 


157 


a  bony  wall  is  formed  which  constitutes  the  greater  bulk  of  the  fetal 
jaw.  The  cavities  in  the  bone  are  called  crypts,  and  are  nicely 
shown  in  Fig.  102,  which  also  shows  the  relation  of  three  permanent 
tooth  sacs  to  those  of  their  predecessors. 


Fig.  96 


:v:^:''..o**vf.' 


..•  •;\ 


I 


r^^V 


Section  of  developing  tooth  of  an  embryo  calf:  a  and  b,  nuclei  of  reticulum  of  enamel  organ, 
showing  spongiose  character;  c,  outer  ameloblastic  membrane;  d,  inner  ameloblastic  mem- 
brane; e  and /,  enamel  globules  faintly  showing  nuclear  network.      X   1000.     (Williams.) 

Fig.  100  shows  a  dental  follicle  in  an  advanced  stage  of  enamel  and 
dentine  development,  viz.,  at  birth.  Root  formation  then  liegins 
and  is  carried  on  by  the  odontoblast.s,  which  build  dentine  against  the 
follicle   walls   at   B,  Fig.    100.     The    first-formed  dentine  contains 


158     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

irregular  spaces  containing  organic  matter  and  collectively  known  as 
the  granular  layer  of  Tomes.  The  tubules  near  this  are  branched 
and  anastomotic.  Coincidently  with  this  the  osteoblasts  in  the  follicle 
wall  deposit  cementum  against  the  dentine  as  a  modified  bone  (sub- 
periosteal deposition)  and  recede,  leaving  some  osteoblasts  in  lacunae. 
The  various  strata  of  cementum  represent  periods  of  incremental  activ- 
ity.    The  follicle  wall  is  caught  between  the  developing  cementum  and 


FiQ.  97 


Section  of  developing  tooth  of  an  embryo  calf:  a,  stellate  reticulum  of  enamel  organ;  6,  stratum 
intermedium:  c,  aineloblasts;  d,  dentine;  e,  odontoblasts;  /,  bloodvessels — corpuscles  in  situ, 
X  275.     (Williams.) 


bone  and  persists  as  a  pericementum,  the  fibers  of  which  attach  them 
to  each  other  (Fig.  10.5).  Fig.  101  shows  the  various  stages  of  root  for- 
mation, the  bifurcation  of  roots  l)eiiig  effected  by  an  upward  pressure 
by  the  follicle  wall  against  the  pulp,  in  the  same  manner  that  the 
enamel  organ  is  indented  by  the  papilla.  The  lower  first  molar  in  Fig. 
110  and  the  third  figure  in  Fig.  101  show  plainly,  by  the  aid  of  a  little 


DEVELOPMENT  OF  THE  TEETH 


159 


imagination,  how  this  is  accomj)Hshed.     The  (hagrani  (Fig.  104)  gives 
the  ages  at  which  root  calcification  is  complete  in  the  temporary  set. 

Fig.  98 


Section  of  growing  tooth  of  calf  at  birth,  showing  fibrils,  fibril  cells,  and  odontoblasts;   also  the 
layer  of  calcoglobulin  and  the  forming  dentine.     (Andrews.) 


Fig.  99 


Mode  of  enamel  deposition:  ^1,  formed  enamel;  B,  amelobla-sts;  C,  secreting  papilla;  of  stratum 
intermedium;  D,  bloodvessels  in  external  fibrous  coat  and  to  secreting  papilla;;  E,  enamel 
globules  with  connecting  plasmic  strings;  F,  nuclei  of  ameloblasts;  G,  blood  supply  of  odonto- 
blastic layer;  //,  odontoblasts;  /,  unformed  dentine;  J,  formed  dentine.  Semidiagrammatic. 
(Williams.) 


160     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

The  Permanent  Teeth. — These  are  nearly  all  formed  from  cords 
given  off  at  the  sixteenth  week  from  the  sides  of  the  cord  of  the  corre- 
sponding temporary  teeth  as  far  back  as  the  bicuspids,  which  are 

Fig.  100 


Developing  tooth  at  birth:  A,  developing  bone;  B,  tissue  reflected  from  follicular  wall  and  form- 
ing alveolar  periosteum;    C,  follicular  wall;  D,  vessels  and  nerves;  E,  epithelium  of  gum. 

given  off  from  the  cords  of  the  first  and  second  temporary  molars;  the 
sacs  are  formed  and  lie  lingual  to  and  above  the  sacs  of  the  temporary 
teeth  at  three  months  after  birth  (Figs.  108  and  109) .  At  the  fifteenth 
week  of  fetal  life  the  cords  of  the  first  permanent  molars  are  given  off 

Fig.  101 


Pulp  cavitie.s  of  the  superior  first  bicuspid,  from  the  seventh  to  the  twelfth  year.     (Broomell.') 

from  the  mucous  membrane,  at  the  third  month  after  birth  the  cord 
for  the  second  molar  is  given  off  from  that  of  the  first  molar,  and  at 
three  years  after  birth  the  cord  of  the  second  molar  arises  from  that 

'  Anatomy  and  Histology  of  the  Mouth  and  Teeth. 


DEVELOPMENT  OF  THE  TEETH 


IGl 


of  the  second  molar.  After  eruption  and  root  completion  in  the 
temporary  teeth  and  some  development  of  the  crowns  of  the  permanent 
teeth  the  relation  of  the  crypts  of  the  permanent  teeth  to  the  temporary 
teeth  is  shown  in  Figs.  107  and  110. 


Fig.  -102 


1,  tooth  sacs  of  deciduous  teeth  turned  out  of  crypts;  2,  Ungual  surface  of  mandible.     The 
interior  of  the  crypts  and  septa  shown.     (Broomell.) 

The  roots  of  the  permanent  teeth  are  developed  during  the  period 
of  their  descent  into  the  alveoli  of  the  temporary  teeth  and  coincidently 
with  the  resorption  of  the  temporary  roots,  which  permits  the  descent. 

Fig.  103 


Section  of  bone  and  periosteum  covering  it:  B,  bone;  c,  outer  fibrous  layer;  a,  inner  layer 
of  white  fibrous  tissue;  O,  layer  of  osteoblasts,  some  of  which  reach  the  bone  with  their  pro- 
longations.    (Black.) 

After  the  shedding  of  the  deciduous  teeth  and  the  eruption  of  the 
permanent  ones  the  roots  are  completed  after  variable  periods,  graphi- 
cally shown  in  Fig.   111.     Coincidently  with  this  the  jaws  enlarge 
11 


162     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 


in  all  directions  by  resorption  and  deposition.  Both  the  develop- 
ment of  the  crowns  and  roots  are  similar  to  those  occurring  in  the 
temporary  teeth. 


Fig.  104 


22  months  after  birth 
18  months  after  birth 


12  montlis  after  birth 


6  months  after  birth 


40th  week  (birth) 
30th  week  embryo 

18th  week  embryo 
17th  week  embryo 


Calcification  of  the  deciduous  teeth.     (Peirce.) 
Fig.  105.  Fig.  106 


Condition   of  third  molar  at  thirteen    years  of 
age.     (Skiagraph  by  Custer.) 


Fig.  107 


Diagram  illustrating  root  development 
and  condition  of  an  incomplete  root:  E, 
enamel;  D,  dentine;  P,  pulp  containing 
odontoblasts,  OB;  A  P,  alveolar  process; 
B,  bone;  C,  cementum;  P^,  periosteum  of 
bone  continuous  with  the  pericementum; 
PER,  pericementum  containing  cemento- 
blasts,  CB;  A,  V,N,  arteries,  veins,  and 
nerves. 


Showing  the  relation  of  pei-manent  tooth  follicle 
to  the  root  of  the  temporary  tooth. 


The  Histology  of  the  Teeth. — Some  of  the  histology  of  the  teeth 
has  been  given  with  the  description  of  the  development  of  the  teeth, 


Fio.  108 


''^'^^ 

*w 

1 

2 

JUi 

^/ 

i '■ 

w* 

Tooth  follicles  for  deciduous  and  permanent  teeth,  three  months  after  birth:  1,  2,  tooth 
sacs  of  deciduous  teeth;  3,  periosteum  of  hard  palate;  4,  tooth  sacs  of  permanent  teeth. 
(Broomell.) 

Fig.  109 


Deciduous  molars  with  tooth  sacs  for  permanent  bicuspids  attached  to  the  gingival  tissue. 

(Broomell.) 


Fig.  110 


View  of  the  upper  jaw  of  a  child,  ancd  aliout  ,~ix  and  one-half  years.  The  anterior  teeth  are 
slightly  separated  by  the  partially  developed  permanent  teeth,  lying  behind  or  posterior  to 
them,  pushing  forward  to  occupy  a  more  anterior  position.  The  equal  height  which  the  crowns 
of  the  deciduous  teeth  originally  occupied  is  also  being  disturbed  by  the  advancing  permanent 
teeth.     (Pierce.) 


164     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 


and  extended  explanation  is  unnecessary  in  a  work  devoted  to  dental 
pathology.     Some  of  the  structures,  however,  require  some  notice  as 
a  basis  for  pathological  variations,  and  will  be  specially  described. 
The  Enamel. — The  rods  radiate  as  shown  in  Fig.  112,  but  in  the 

fissures  Nasmyth's  membrane 
persists  and  rarely  completes  a 
perfect  groove,  so  that  a  con- 
venient location  for  food  and 
microorganisms  remains,  and 
dental  caries  is  most  common  at 
this  point.  The  enamel  is  thin 
at  the  cervix  and  is  usually  over- 
lapped by  the  cementum,  but 
may  overlap  it  or  lie,  edge  to 
edge,  with  it  (Choquet).  The 
striae  of  Retzius  are  pigmented 
bands,  incremental  in  charac- 
ter. The  stripes  of  Schreger 
are  cloud-like  markings,  shown 
by  Caush  to  be  due  to  the  pres- 
ence of  tubes  in  the  enamel 
and  containing  organic  matter. 
The  Dentine. — ^The  tubules 
are  curved  in  outline  and  some- 
times show  a  series  of  short, 
sharp  curves  on  a  general 
curved  level  at  the  points  at 
which  a  new  period  of  incre- 
ment has  occurred.  They  are 
the  stripes  of  Schreger  in  den- 
tine or  "incremental  lines"  of 
Salter. 

The  Pulp. — This  consists  of 
a  gelatinous  matrix  in  which 
are  embedded  branched  con- 
nective-tissue cells.  The  odon- 
toblasts lie  upon  its  surface 
next  to  the  dentine,  with  their 
fibrils  extending  into  the  tubules 
up    to    the    enamel,    and,    as 


HISTOLOGY  OF  THE  TEETH 

Fig. 112 


165 


Diagram  of  enamel-rod  directions  and  tubule  curves.     From  a  photograph  of  a  buccolingual 
section  of  a  superior  bicuspid.     (No.ves.) 

Fig,  113 


Section  of  enamel  of  luiman  tooth.  Photographed  with  Zeiss  apochromatic  lens  and  Powel 
and  Leland  apochromatic  condenser.  The  optical  parts  accurately  centred  and  the  focus 
'critical."  The  enamel  rods  are  seen  to  be  resolved  into  distinct  sections  (enamel  globules), 
the  cement  substance  often  passing  entirely  between  the  sections.      X  400.     (Williams.) 


166     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

shown  by  Caiish,  often  into  it,  forming  organic  matter  in  enamel, 
and  in  some  cases  accounting  for  a  sensitivity  which  is,  however, 
rare. 

Fig.  114 


Enamel  prisms :  A ,  fragments  and  single  fibers  of  the  enamel  isolated  by  the  action  of  hydro- 
chloric acid;  B,  surface  of  a  small  fragment  of  enamel,  showing  the  hexagonal  ends  of  the 
fibers.      X  350. 

Fig.  115 


Enamel  showing  both  atriation  and  stratification.      X  80  (about).      (Noyes.) 


One  or  more  arteries  enter  the  apical  foramen  or  by  several  fora- 
mina, antl  several  veins  may  emerge.  The  arteries  subdivide  in  the 
central  portion  of  the  pulp  and  form  a  rich  network  of  capillaries 
beneath  the  odontoblasts. 


IIlSrOLOGY  OF  THE  TEETH 
Fig.  116 


167 


lo    p  o 


'©• 


.*"    Oa*    ^^•^^       ,^^-.     *• 


Transverse  ground-section  through  the  dentinal  tubules  of  the  first  molar  of  a  child 
years:     V,  Koch's  and  Golgi's  methods  combined.      X  1200.     (Rose.) 

Fit:.  117 


CD. 


U.D. 


P.O. 


K% 


^  stifle 


"^'^^#fU!^ 


i'^ 


^ 


^  ■ 


.^rrl 


Section  of  pulp,  showing  the  relations  of  the  odontoblasts  to  the  dentine:  Od.,  odontoblasts; 
T.F.,  Tomes'  fibers — odontoblastic  processes;  U.D.,  uncalcified  dentine;  CD.,  calcified  dentine; 
P.C.,  pulp  cells.      X  800.     (Rose  and  Gysi.) 


168     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

The  arteries  of  the  pulp  soon  lose  almost  entirely  their  muscular 
coat,  and  their  external  coat  is  reduced  to  an  inconsiderable  amount 
of  fibrous  connective  tissue.  There  is  little  if  any  anastomosis  of  the 
arteries  of  the  pulp,  so  that  collateral  circulation  is  impeded,  though 
not  necessarily  prevented,  as  pathological  cases  show.  The  veins 
remain  for  an  unusual  distance  without  a  muscular  coat,  and  are  stated 
by  Hopewell-Smith  to  be  non-valvular  and  non-collapsible.^  This 
histological  datum  has  great  clinical  significance.  (See  Diseases  of 
the  Pulp.) 

Fig.  118 


Main  mass  of  dentine  of  a  temporary  tooth,  stained  with  chloride  of  gold,  decalcified  with 
acetic  acid:  F  F,  dentinal  fibers,  partly  vacuolated;  i?  .S,  basis  substance,  traversed  by  a  reticu- 
lum.     X  1200.     (Hart.) 

The  vascularity  of  the  pulp  decreases  with  age.  "In  young  teeth 
there  are  a  number  of  arterial  trunks  entering  the  apical  foramen, 
which  lessen  in  number  as  the  passage  lessens  in  size."  Finally  only 
one  may  enter  (Black). 

The  passage  of  arteries  and  veins  through  a  constricted  foramen 
has  important  consideration  in  connection  with  pulp  diseases.  (See 
Venous  Hyperemia  of  the  Pulp.) 

The  nerves  enter  by  several  bundles,  and  if  medullated  soon  lose  the 

•  Dental  Cosmos,  1907. 


HISTOLOGY  OF  THE  TEETH 


169 


medullary  sheath.  They  are  derived  from  the  trigeminus  and  the 
sympathetic  system. 

Those  from  the  sympathetic  are  (Hstributed  to  the  bloodvessels  as 
vasomotors;  the  others  form  a  plexus  in  intimate  relation  with  the 
odontoblasts.  They  have  been  found  by  Retzius  to  terminate  in 
knob-like  extremities  between  the  odontoblasts  in  the  mouse.  These 
are  probably  sensory  nerves. 

No  direct  anatomical  connection  has  been  made  out  between  the 
nerve  fibers  and  the  odontoblasts  or  the  fibrillfe,  although  Robertson 

Fig.  119 


\     \  \  \ 


D 


Ground-section  through  the  root  of  a  human  premolar:  D,  dentine;   A',  cement  corpuscles;  O, 
osteoblasts;   Ep,  pericemental  glands  of  Black;"  ./,  interglobular  spaces.      X  200.     (Rose.) 

has  claimed  to  have  traced  the  long  central  fiber  running  from  the 
odontoblasts  into  the  pulp  into  nerve  bundles  and  claims  that  they 
become  axis  cylinders.  The  phenomenon  of  sensitive  and  hyper- 
sensitive dentine  shows  an  evident  physiological  connection.  The 
nerves  of  the  pulp  do  not  possess  tactile  sense,  so  their  pains  are 
not  localized  but  reflected  as  a  rule.  The  pulp  contains  no  demon- 
strable lymphatics,  though  lymph  spaces  probably  exist ;  their  office  is 


'  The  editor  has  taken  the  liberty  of  altering  the  interpretation. 


170     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

probably  performed  bj  the  veins,  which  in  other  parts  may  take  up 
this  function.^  The  pulp  becomes  more  fibrous  and  less  vascular 
with  age.  During  health  it  preserves  the  translucency  of  the  tooth, 
tlirous-h  its  relation  with  the  fibrillse  and  under  certain  circumstances 
renews  its  formative  activity  and  produces  secondary  dentine.  The 
forms  of  the  pulps  and  pulp  cavities  are  shown  in  Figs.  123  to  132. 


Fig.  120 


■N.F. 


S.D.- 


Od.- 


N.T.- 


B.V.- 


C.6 


Sectiiju  (jl  .i  luoil,  juilp  Al  ,  liiaiii  bl(M)(h(~Ml- (jf  iiulii,  <•  ,  nr  i^m  <il  <  ipiH^n  ics,  \  7' ,  iii.iiii 
nerve  trunk.  A''  F  .  subclI\l'^lons  of  nerve  into  hbiillj";  Od  ,  odontobla'^tic  la>ei ,  S  D  ,  secondaiy 
dentine;  C.G'.,  masses  of  oalcoglobulin.      X  30.     (Rose  and  Gysi.) 

The  Cementum. — The  cementum  is  a  modified  bone  distributed 
over  the  dentine  of  the  root.  It  meets  the  enamel  either  edge  to  edge 
overlaps  it,  or  is  overlapped  by  it  (Chaquet). 

The  physiological  function  of  the  cementum  is  to  afford  a  means 
of  attachment  of  the  teeth  to  the  maxillary  bones  through  the  medium 
of  the  pericemental  fibers.  In  case  of  death  of  the  pulp,  and,  there- 
fore, of  cessation  of  nutrition  of  the  dentine,  the  vital  relations  of  the 
cementum  and  alveolar  process  are  thus  maintained  and  the  useful- 
ness of  the  tooth  assured.     Whether  the  dentine  can  ever  receive 

1  Green's  Patliology  and  Morbid  Anatomy. 


HISTOLOGY  OF  THE  TEETH 


171 


nourishment  from  the  cementura  after  pulp  death  has  never  been 
scientifically  shown,  and  the  fact  that  it  contains  dead  and  even 
putrified  material  while  a  healthy  cementum  may  persist,  renders  it 
extremely  doubtful. 

The    Pericementum. — {Syn.    Peridental    Membrane.) — The  peri- 
cementum is  the  liiglily  organized  remains  of  the  follicle  wall.     As 

Fi(i.  121 


^-%^ 


Two  fields  <it  (•(Miientmii,  slidwing  peiiotiatiiiK  fibers:  Gt..  luramilar  layer  of  'I'omes;  ('.,  rementum 
not  showing  fibers;   F.,  penetrating  fibers.      X  54   (about).     (Noyes.) 

the  alveolar  bone  and  cementum  develoj)  on  either  side  of  it,  it  forms 
also  the  periosteum  lining  the  alveolus.  It  is,  therefore,  the  means  i)y 
which  the  teeth  are  retained  in  tlieir  sockets  and  a  certain  desrree  of 
motion  permitted.  The  pericementum  subserves  the  office  of  a 
membranous  attachment  not  altogether  unlike  that  foinid  in  the 
sutures  of  the  cranial  bones. 

It  is  considered   by  some  observers   that   there   are   two  distinct 


172     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

portions  to  the  pericementum,  cemental  and  alveolar.  Photo- 
micrographs generally  do  not  demonstrate  this,  and  it  is  a  matter  of 
difficulty  to  imagine  the  pericemental  bands  divided  into  two  portions. 

It  is  continuous  with  the  periosteum  on  the  outside  of  the  alveolar 
process,  as  the  sutural  membrane  is  with  the  pericranial  membrane. 

Its  outline  study  divides  the  pericementum  into  three  portions: 
a  gingival,  an  alveolar,  and  an  apical  portion.^ 

Fig.  122 


Portion  of  the  side  of  a  root  of  a  tooth,  the  gum  and  aiveolodental  membrane,  and  the  edge 
of  the  bone  of  the  alveolus.  A  band  of  fibers  is  seen  passing  over  the  surface  of  the  alveolus 
and  dividing,  some  passing  upward  into  the  gum,  others  passing  more  directly  across  to  the 
cementum.  Numerous  orifices  of  vessels  cut  across  transversely  are  seen  between  the  tooth 
and  the  bone.     (Black.) 

It  is  composed  largely  of  white  fibrous  tissue  with  interlaced  blood- 
vessels, nerves,  and  glands.  It  also  contains  functional  cells,  fibro- 
blasts, cementoblasts,  osteol)lasts,  and  osteoclasts. 

The  fibrous  tissue  is  made  up  of  principal  fibers  and  indifferent 
fibers.^ 

The  principal  fibers  are  grouped  for  the  most  part  in  bands  or 
bundles. 

In  the  alveolar  portion  these  bundles  run  for  the  most  part  from 


'  Noyes,  American  Text-book  of  Operative  Dentistry. 


«Ibid 


HISTOLOGY  OF  THE  TEETH 


173 


the  cementum  to  a  higher  point  on  the  alveolar  process.     The  attach- 
ment is  secured  by  the  penetration  of  the  fibers  into  either  structure. 


Fig.  123 


Fig.   125 


Fig.   127 


Fig.   129 


Fio.  124 


Fig.   126 


Fig.   128 


Fig.   130 


Longitudinal  and  transverse  sections  of  upper  teeth,  showing  shapes  of  pulp  chambers 

and  their  positions. 

This  secures  to  the  tooth  support  against  direct  pressure  into  the 
socket  and  against  rotary  motion. 

At  the  apical  portion  the  bands  have  a  fan-like  distribution.     In 


174     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

Fig.  131 


Formalin-gelatin  casts  of  pulp  cavities,  showing  pulp  irregularities.      (Richards.) 

Fig.  132 


Formalin-gelatin  casts  of  pulp  cavities  compared  with  the  teeth  themselves.     (Richards.) 


HISTOLOGY  OF  THE  TEETH 


175 


the  gingival  portion  the  fibers  are  (hrected  outward  and  shghtly 
downward  for  attachment  to  the  process,  or  outward  and  downward 
over  the  i^dge  of  the  process  to  become  continuous  with  the  periosteal 
fibers,  or  outward  and  upward  with  the  submucous  gingival  tissue  to 
aid  in  the  support  of  the  gum  margin.  Some  of  the  gingival  fi})ers 
pass  from  the  cementum  of  one  tooth  to  that  of  the  next. 


KiG.  133 


wing  the  buccal  surfaces  of  the  crowns  and  roots  in  position.     (Cryer.) 


The  l)loodvessels  of  the  pericementum  are  derived  from  several 
sources:  (1)  From  several  vessels  derived  from  a  single  trunk  entering 
the  apical  space  from  the  bone  above;  (2)  from  vessels  entering  the 
membrane  through  the  Haversian  canals  of  the  alveolar  process  and 
anastomosing  with  branches  from  the  descending  arteries;  (3)  from 
the  vessels  of  the  outer  periosteum,  coming  over  the  edge  of  the 
alveolar  process. 


176     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

There  are  comparatively  few  capillaries.     The  vessels  lie  mostly  in 
the  outer  or  alveolar  half  of  the  pericementum. 

This  disposition  of  the  arterial  blood  supply  ensures  nutrition  to 


Fig.  134 


Vertical  section  of  a  frozen  head,  rear  view.  Shows  relations  of  roots  of  molars  and  the 
maxillary  sinus,  and  of  the  maxillary  sinus  with  the  frontal  sinus.  Wire  passes  from  the  latter 
through  the  infundibulum,  the  hiatus  .''emilunaris,  and  the  ostium  maxillare,  into  the  maxillary 
sinus,  establishing  a  connection.     (Cryer.) 


HISTOLOGY  OF  Till':  TEETH  177 

the  peridental  ineiiil)raiie  in  case  of  loss  of  the  aj)ical  tissue,  as  incase 
of  apical  abscess,  and  also  insures  a  colhiteral  Ijlood  supply  to  the 
pulps  in  case  of  loss  of  main  arterial  trunks,  as,  for  example,  in 
operations  upon  the  inferior  dental  canal. 

The  arteries  thus  furnishing  blood  to  the  teeth  are,  for  the  upper 
jaw:  the  anterior  dental  branch  of  the  infra-orbital,  to  the  upper 
anterior  teeth;  tiie  su})eri()r  dental  branch  of  the  alveolar,  to  the  upper 
bicuspids  and  molars  and  the  bone  about  their  root  ends;  the  de- 
scending palatine  and  its  anastomotic  connection,  the  sphenopalatine, 
supplied  to  the  palatine  side  of  the  upper  alveolar  process,  etc. ;  the 
alveolar,  supplied  to  the  buccal  side  of  the  upper  alveolar  process. 

In  the  lower  jaw  the  inferior  dental  arterv  and  its  incisor  branch 
supply  the  apical  tissues  of  the  lower  teeth  from  the  inferior  dental 

Fig.  135 


Diagram  if  ulaiids  of  jipiidpntal  nipnibrane.     (Black.) 

canal.  Its  mylohyoid  branch  supplies  the  gums  and  lingual  j)erios- 
teum  of  the  lower  alveolar  process,  the  mental  branch  supplies  the 
lower  buccal  process  anteriorly,  while  a  !)ranch  of  the  facial  artery 
anastomoses  with  the  mental  anteriorly,  and  the  facial  sends  branches 
to  the  coverings  of  the  buccal  aspect  of  the  lower  jaw  posteriorly. 
With  the  exception  of  tho.se  branches  derived  from  the  facial  art(>ry, 
all  the  blood  comes  from  the  internal  maxillary  artery. 

The  veins  r(>turn  {\\v  blood  by  similar  channels. 

The  nerves  of  the  pericementum  enter  by  several  trunks  in  the 
apical  ti.ssue  and  also  enter  from  the  alveolar  wall  and  over  the  alveolar 
edge.  While  their  distribution  is  not  vet  fullv  described,  some  of 
12 


178     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

them  possess  the  tactile  sense,  as  touch  upon  the  teeth  is  fully  localized. 
They  are  derived  from  the  fifth  nerve  and  the  sympathetic. 

The  Pericemental  Glands. — ^Black  has  described  gland-like  structures 
lying  in  the  pericementum  nearer  the  cementum  than  the  alveolar  wall. 
These  are  distributed  over  the  root  in  a  network,  as  shown  in  Fig.  135. 

They  are  convoluted  cords  of  epithelial  cells  invested  with  a  delicate 
basement  membrane,  and  can  be  traced  to  the  epithelium  of  the  gin- 
gival space,  but  not  to  the  surface. 

Fig.  136 


Glands  of  Black.     Epithelial  structures:  Ec,   epithelial  cord,   apparently  showing  a  lumen; 
Cb,  cementoblasts;   Cm,  cementum;  D,  dentine.      X  500  (about).     (Noyes.) 

Traces  of  a  lumen  have  been  seen,  which  if  established  as  common 
would  constitute  them  as  tubes.  Their  function  is  not  definitely 
known,  but  it  is  presumptive  that  they  are  either  secreting  glands  or 
lymphatics.  The  entrance  of  l)acteria  from  the  gingival  space  to  deep 
portions  of  the  pericementum,  there  to  develop,  may  possibly  be 
favored  by  their  presence  (Figs.  119,  135,  and  130). 

Glands  of  Series. — At  the  deepest  portion  of  the  gingival  space 
is  f(Mind  a  glan<l-lil«'  body  which  has  been  given  the  above  name. 
Its  fuiiction  is  not  known  (Fig.  137). 


Fig.  137 


Longitiiiliiial  section:  Ep,  epitlielium  liiiiiiR  tlio  n'"E'\'i'  '^liai.'p;  (.la,  Ki'ieival  eland,  so-oalled; 
D,  dentine;  A^,  Nasmyth's  nienihrane;  /)«.  3uct-like  structure  stretchinR  away  toward  the  gin- 
givus  from  the  epithelial  cord,  seen  at  Ec;  Cm,  cementum,  separated  from  the  dentine  by  decal- 
cification.    X  50  (about),     (Noyes.) 


180     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

The  Cellular  Elements. — The  fibroblasts  are  spindle-shaped  cells 
destined  to  become  mature  fibers.  They  lie  among  the  other  fibers. 
The  cementoblasts  lie  along  the  cementum  and  are  the  cementum 
builders  (Figs.  103  and  105).  Osteoblasts  are  found  engaged  in 
bone  construction  along  the  alveolar  wall. 

Osteoclasts,  large  multinucleated  cells,  lie  at  points  along  the 
cementum  of  teeth  and  alveolar  bone.  Their  office  is  the  removal  of 
bony  tissue.  They  remove  both  the  organic  and  inorganic  material, 
and  their  effects  are  seen  upon  the  cementum  and  dentine  of  the 
roots  of  teeth  undergoing  resorption,  also  upon  resorbed  alveolar 
process.  The  excavations  in  which  they  lie  at  work  are  called  How- 
ship's  lacunae  (Fig.  73) . 

Calcospherites  are  sometimes  found  within  the  substance  of  the 
pericemental  membrane,  and  may  have  some  significance  in  relation 
to  its  diseases. 

The  pericementum  in  the  young  is  comparatively  large  and  vascular, 
and  in  the  old  becomes  much  attenuated,  more  fibrous,  less  vascular, 
and  subject  to  degeneration. 

Union  of  alveolar  bone  and  cementum  but  rarely  occurs,  though  a 
mechanical  attachment  by  fibrous  pericementum  may  occur.  (See 
Synostosis.)  On  the  other  hand,  the  union  of  the  cementum  of  one 
tooth  with  that  of  another  is  not  uncommon.      (See  Concrescence.) 


CHAPTER    VII. 

DEXl^ITION:  ITS  PROGRESS,  VARIATIONS,  AND  ATTENDANT 

DISORDERS. 

The  process  of  teething,  eruption,  or  dentition  comprises  that 
series  of  vital  operations  which  cause  the  teeth  to  leave  their  crvpts 
in  the  maxillre,  to  pierce  the  gum,  and  to  take  tlieir  j)laces  in  the 
dental  arches.  It  is  a  continuation  of  the  process  of  dental  develop- 
ment, and  is  accompanietl  and  succeeded  by  root,  alveolar,  and  max- 
illary developments,  which  are  also  to  be  considered  in  connection 
with  it. 

Physiologically  dentition  is  divided  into:  (1)  the  first  dentition,  or 
that  of  the  tem})orary  teeth;  (2)  the  second  dentition,  or  that  of  the 
permanent  teeth. 

Examination  of  Fig.  100  will  show  the  state  of  tooth  development 
at  a  period  shortly  after  birth  (a  central  incisor  being  under  con- 
sideration). The  crypt  is  roofed  over  at  birth  by  a  membranous 
structure.  During  the  j)eriod  from  then  to  perhaps  six  months  after 
birth  about  one-third  of  the  root  will  have  been  formed.  (See  Fig. 
104.)  The  root  end  is  widely  open  (incomplete)  and  the  margins  are 
thin  and  sliarp.  A  very  vascular  tissue  occupies  the  space  between 
the  root  and  the  bone  and  fills  the  interior  of  the  root.  ]\Ieanwhile 
the  crown  cusp  will  have  advanced  from  the  situation  shown  in  Fig. 
100  to  a  point  just  beneath  the  mucous  membrane,  Avhich  is  pressed 
Uj)  and  stretched  over  the  advancing  tooth  crown,  presenting  to  oral 
view  a  tumefied  condition  more  or  less  corresponding  to  the  form  of 
the  crown.     This  is  nicely  shown  in  Fig.  13S,  A  and  li. 

These  anatomical  data  serve  for  the  consideration  of  the  causes 
and  ])rocess  of  eruption. 

Causes  of  Eruption. — It  is  evident  that  there  are  forces  wiiich 
can  bring  about  the  elevation  of  a  tooth  crown  from  its  bed  in  the 
crypt  to  its  j)()sition  in  {\\v  mouth. 

I'he  consideration  of  these  has  caused  the  development  of  the 
following  rational  theories,  as  w(>ll  as  others  now  obsolete. 

1.  That  crown  elevation  is  due  to  the  lengthening  of  the  root — 
i.  r.,as  root  ti.ssue  is  formed  by  the  pulp  and  follicle  wall  lying  beneath 


182  DENTITION 

and  to  the  side  of  its  edges,  the  tooth  is  mechanically  pushed  up, 
more  root  is  formed,  and  a  further  extrusion  occurs.  It  is  to  be 
noted  that  the  root  end  occupies  the  same  level,  at  all  stages  of  eruption, 
in  the  developing  jaw  that  was  occupied  by  the  cervical  edge  of  the 
crown  (Fig.  139).  As  no  two  bodies  may  occupy  the  same  space  at  the 
same  time,  the  root-forming  pulp  and  follicle  wall  push  the  tooth  up  to 
gain  room  for  more  root  formation.  The  mild  continued  press- 
ure is  quite  competent  to  do  this.  The  pressure  of  the  soft  tissues 
against  the  root  end  is  explained  by  Constant  to  be  derived  from  the 
normal  blood  pressure.^  That  such  an  internal  pressure  exists  is 
shown  by  the  extrusion  of  ordinarily  confined  parts  when  released 
from  the  accustomed   pressure.     A  simple    accident  demonstrated 

Fig.  138 


Lines  of  incision  in  lancing:  A,  A,  over  the  molars;  B,  B,  over  the  cuspids  and  incisors 
before  eruption;  C,  C,  over  the  molars  and  cuspids  after  partial  eruption. 

this  to  the  editor.  While  excavating  with  a  large  bur  the  softened 
dentine  about  a  decayed  pulp  chamber,  the  cementum  was  widely 
removed  from  the  pericemental  tissue  beneath,  which  latter  fortunately 
remained  unbroken.  It  immediately  protruded  into  the  perforation. 
Constant  also  cites  the  extrusion  of  a  tooth  in  pericementitis  as  an 
evidence  of  the  influence  of  the  blood  pressure.  Another  evidence  is 
the  occasional  rapid  advance  of  a  tooth  after  lancing  of  the  gum. 

2.  The  process  of  tooth  development  is  a  vital  process,  and  that 
of  eruption  has  been  held  also  to  be  (Tomes).  .  That  cells  concerned 
in  development  seem  to  have  a  predestined  end  or  function  cannot  be 
denied;  at  the  same  time,  throughout  dental  development,  defined 
resistances  to  opposing  forces  seem  to  play  a  part  in  the  moulding  of 
the  soft  and  liai'd  tissues — e.  g.,  the  dej)ression  of  the  enamel  organ 
by  the  papilla. 

•  International  Dental  Journal,  Juno,  1903. 


DENTITION 


183 


3.  Pierce'  holds  that  tlie  impact  of  l)l()\v.s  upon  the  jaws  causes  the 
tooth  to  rise  toward  the  gum.  lie  ex})hdns  the  eruption  of  crowns 
without  roots  upon  tliis  theory. 

4.  Tomes  expUiins  the  eru])tion  of  teeth,  after  development  of  the 
root,  upon  the  theory  that  the  closing  in  of  the  alveolar  process  or 
contraction  of  the  alveolus  upon  the  pericementum  (follicle  wall) 
causes  the  lifting  up  of  the  tooth.  That  such  a  clo.sure  occurs  about 
the  extruding  roots  of  teeth  left  after  the  breaking  away  of  the  crowns 
is  shown  by  examination  of  the  sockets  of  such  roots.  An  abnormally 
shallow  alveolus  closcfl  by  deposition  of  bone  at  its  apex  will  be  found 
in  cases  of  small  apical  portions  of  roots  so  extruded.  Upon  the 
whole,  Constant's  theory  of  l^lood  pressure  seems  the  most  satisfactory 
explanation  of  tooth  elevation  under  any  circumstances. 


Fig.  139 


Diagram    showing   the   upward  movement  of   the   prown  during  eruption  and 
root  development.     (Constant.) 

It  is  well  known  that  mild  hy{)eremia  is  j)ro(hiced  in  pericementi 
which  do  not  receive  a  normal  resistance,  which  would  account  for 
both  the  elevation  and  bont^  deposition.     (See  Arterial  Hyperemia.) 

The  Process  of  Dentition. — At  varying  ages,  acconh'ng  to  the 
state  of  tooth  developnuMit,  {\\v  formed  crown  of  the  tooth  advances 
and  presses  upon  the  follicle  wall  overlying  it;  this  is  resorbed,  the 
overlying  tissue  is  reached,  and  osteoclasts  (giant  cells)  remove  this 
as  well  as  the  upper  Qi\ge  of  the  wall  of  the  crypt;  the  mucous  mem- 
brane is  pushed  up  and  mouMcd  over  the  crown,  thereby  causing  a 
tumefaction. 

The  mucous  memi)rane,  at  first  normal  in  color,  becomes  slightly 
hyperemic,  and  then  may  change  to  an  ischemic  condition  and  whiten 
owing  to  the  removal  of  the  blood  by  the  pressure  of  the  underlying 

'  American  System  of  Dentistry. 


184  DENTITION 

crown.  Resorption  from  beneath  causes  a  break  in  the  continuity  of 
the  mucous  membrane,  and  the  crown  tip  erupts  into  the  mouth 
(Fig.  138,  C). 

The  rate  of  resorption  and  crown  advance  are  equaUzed  in  perfectly 
normal  dentition. 

The  crown  rises  from  the  gum,  is  directed  by  the  tongue  and  lip 
or  cheek,  and,  finally,  meets  its  antagonists  of  the  opposite  jaw.  The 
interlocking  of  cusps  and  meeting  of  occlusal  surfaces  limit  further 
movement  of  position. 

Meanwhile  root  development  proceeds,  and  as  it  occurs  the  alveolar 
process  is  built  about  the  pericementum,  which  has  been  drawn  up 
from  the  follicular  wall.  By  this  means  the  roots  are  firmly  implanted. 
The  further  development  of  the  root  proceeds  until  complete,  and  so 
remains  until  normal  resorption  of  the  temporary  roots  occurs,  and  for 
life  in  the  permanent  teeth. 

The  state  of  formation  of  the  roots  of  temporary  teeth  at  any 
given  age  may  be  judged  by  the  table  of  averages  shown  by  Peirce 
in  Fig.  104.     Being  but  averages,  allowance  for  delays  must  be  made. 

Apart  from  the  presence  of  the  temporary  teeth  the  process  of 
eruption  is  identical  in  both  sets  of  teeth. 

Periods  of  Eruption. — ^As  a  general  rule,  the  eruption  of  the 
deciduous  teeth  may  be  said  to  begin  about  the  seventh  month  after 
birth,  and  is  completed  somewhere  about  the  twenty-fifth  month. 
This  rule,  however,  varies  within  wide  limits;  some  children  may  be 
born  with  teeth  erupted;  again,  the  initiation  of  the  process  may  not 
occur  until  the  twelfth  month  or  even  later. 

The  incisor  teeth  are  usually  erupted  in  pairs,  the  molars  and 
cuspids  making  their  appearance  in  fours,  the  first  molars  in  one  group, 
the  cuspids  in  another,  and  the  second  molars  in  a  third  group.  The 
several  groups  require  different  lengths  of  time  to  complete  their  erup- 
tion, the  time  occupied  in  the  eruption  of  the  first  molars  being  longer 
than  that  recjuired  for  the  eruption  of  the  other  groups.  Between  the 
appearance  of  additional  groups  of  the  teeth  an  interval  elapses,  no 
doubt  a  physiological  provision,  for,  as  will  be  shown  later,  the  process 
of  dentition  is  usually  accompanied  by  evidences  of  more  or  less  local 
disturbance,  frequently  by  disturbances  throughout  the  intestinal  tract, 
and  even  reflex  disorders  of  the  central  nervous  system  occur.  It  is 
Ix'lieved,  therefore,  that  the  period  which  elapses  between  the  eruption 
of  the  dental  groups  permits  the  organism  to  recover  from  tlic  effects 
of  previous  disturbance  before  the  new  source  of  irritation  appears. 


DEXTITIOX 
Table.^ 


185 


Group 

1. 

Lower  central  in- 

Time of  eruption, 

Duration  of  eruption, 

Interval,  2  to  3  months. 

cisors. 

7  montlis. 

1  to  10  days. 

Group 

2. 

Upper  central  and 

Time  of  eruption, 

Duration  of  eruption. 

Interval,  2  months. 

lateral  incisors. 

9  months. 

4  to  6  weeks. 

Group 

3. 

Lower  lateral  in- 
cisors. 

Time  of  eruption, 
12  monihs. 

Group 

1. 

Fii.-it  molars. 

Time  of  erujjtion, 
14  months. 

Duration  of  eruption, 
1  to  2  months. 

Interval,  4  to  .5  months. 

Group 

5. 

Cuspids. 

Time  of  eruption, 
18  months. 

Duration  of  eruption, 
2  to  3  months. 

Inter\'al,  3  to  5  months. 

Group 

(i. 

Second  molars. 

Time  of  eruption, 
26  months. 

Duration  of  eruption, 
3  to  5  months. 

In  the  above  table  it  will  be  noted  that  th(>  time  of  eru])tion  of 
the  lower  lateral  incisor.s  is  later  than  that  of  tlu>  eruption  of  the  upper 
lateral  inei.sor.s.  The  reverse  course  is  fre(juently  observed;  indeed, 
it  has  usually  l)een  accepted  as  the  rule  of  precedence  in  the  United 
States.  All  tables,  as  to  periods  of  eru})ti()n,  i^Wv  but  the  approximate 
times;  while  variations  are  extremely  common.  The  ages  given  in 
this  table  are  those  at  about  which  the  several  teeth  may  be  expected 
to  make  their  appearance.  Stellwagen  (the  American  editor  of 
Coleman),  in  commenting  u])on  this  table,  states  that  the  periods  of 
eruption  in  this  country  are  from  one-seventh  or  more  earlier  than  the 
dates  given.  He  suggests  that  the  difference  in  food-habit  may 
account  for  the  diti'erences  in  time. 

Pari  passu  with  the  development  and  eruption  of  the  teeth  occur 
developmental  changes  in  all  of  the  glandular  a])pendages  of  the 
alimentary  canal;  probably  the  alterations  in  their  structure,  and  no 
doubt  in  their  ])hysi()logieal  chemistry,  are  accompanied  by  dental 
provision  for  the  mechanical  subdivision  of  foods  of  ])ostinfantile 
character. 

Symptoms  of  Eruption. — Slight  local  distiirbances  are  so  common 
in  even  so-called  normal  first  dentition  as  to  be  accepted  as  physiologi- 
cal. The  resorption  of  soft  tissue  around  the  ti])  of  the  crown  of  the 
tooth  implies  a  condition  of  mild  non-septic  inflammation  at  that  ])oint. 
In  more  marked  castas  there  is  evidence  of  some  irritation  cognizable  to 
the  infant;  the  gum  is  of  a  somewhat  deeper  color  and  its  temperature 
is  elevated.  Relief  is  afforded  by  pressure,  which  temporarily  reduces 
the  hyperemia,  and  the  child  is  pleased  to  have  its  gums  rubbed,  to 
bit(>  upon  its  own  or  {hv  nurse's  fingers,  upon  rings  or  otlier  objects. 
Still  more  marked  is  the  soothing  effect  of  biting  u])on  cold  substances 


'  Coleman's  Dental  Surscry.      (Slollwat;en). 


186  DENTITION 

such  as  ice,  which,  in  addition  to  mechanically  lessening  the  blood 
supply,  causes  contraction  of  the  dilated  vessels. 

Slight  reflex  disturbances  are  evidenced  by  the  stimulation  of  the 
salivary  glands,  which  produces  an  increased  flow  of  saliva. 

Reflex  disturbances  of  more  severe  character  occur  in  pathological 
dentition,  to  be  considered  later. 


PATHOLOGICAL  FIRST  DENTITION. 

The  local  disturbances  may  be  exaggerated  beyond  that  degree 
accepted  as  physiological  and  may  be  accompanied  by  nervous,  ali- 
mentary, pulmonary,  or  cutaneous  disturbances.  This  is  pathological 
dentition,  and  may  be  of  several  grades  of  severity. 

Causes  and  Pathology. — The  primary  cause  of  pathological  dentition 
may  be  stated  as  an  inequality  in  the  rate  of  gum  resorption  and 
crown  advance.  The  advancing  crown  pressing  upon  the  gum  tissue 
causes  irritation;  the  hyperemia  or  mild  aseptic  inflammation  resulting, 
instead  of  remaining  at  a  point  favoring  the  development  of  giant  cells 
and  resorption,  passes  the  physiological  point  and  causes  a  disturbance 
of  function.  Inflammation,  simple  or  even  infective,  may  occur  in 
the  area. 

Swelling  of  the  gum  occurs,  which,  being  distributed  in  all  directions, 
presses  upon  the  crown,  depressing  it  upon  the  pulp  beneath  the 
sharp  root  margins;  at  the  same  time  the  blood  pressure  of  the  pulp 
tends  to  press  the  tooth  upward.  The  simple  lack  of  resorption  of 
the  gum  would  be  almost  equally  effective  in  preventing  eruption. 

The  sharp  edges  of  the  root  must  irritate  the  sensitive  and  delicate 
pulp  tissue,  which  becomes  inflamed  and  swollen  and  still  more 
strongly  urges  the  tooth  upward.  Two  sources  of  disturbance  now 
are  possible:  (1)  The  irritated  gum  tissue  and  (2)  the  irritated  pulp. 
The  latter  is  the  more  likely  to  cause  reflex  disturbances.  Through 
the  intimate  sympathetic  relations  of  the  fifth  cranial  nerve,  supplied 
to  the  pulp,  with  the  seventh,  ninth,  and  tenth  cranial  nerves  in  the 
floor  of  the  fourth  ventricle  of  the  brain,  salivary,  muscular,  nervous, 
alimentary,  aud  pulmonary  disturl)ancos  become  possil^le. 

Though  the  pulp  is  more  likely  to  produce  the  reflex  disturbance, 
a  gum  inflammation,  if  intense,  is  often  capable  of  producing  even 
prostrating  symptoms.  Any  systemic  disturbance — e.  c/.,  smallpox, 
general  debility,  or  lesser  disturbance,  etc. — which  lowers  the  gen- 


PATHOLOGICAL  FIRST  DEXTITIOX  187 

eral  nutritive  function  also  in  the  parts  associated  witli  the  teeth 
may  favor  the  production  of  local  pathological  phenomena.  Again, 
systemic  disturbance  readily  produces  a  hyperesthesia  of  the  nervous 
system,  favoring  the  production  of  nervous  phenomena. 

Pathological  dentition  may  occur  in  the  absence  of  an  evitlent 
hy])eremic  gimi  tissue.  The  tissue  may  be  white,  showing  ischemia 
from  pressure,  a  binding  down  of  the  root  end  upon  the  pulp  being 
proved  by  the  subsidence  of  symptoms  after  lancing,  and  sometimes 
by  the  rapid,  partial  eruption  of  the  tooth  immediately  after  lancing. 

Again,  pathological  phenomena  have  been  noted  where  no  super- 
ficial local  disturbance  was  evident.  In  these  cases  the  deeper  tissues 
may  exert  a  restraining  influence  upon  the  crown,  but  the  swelling  is 
just  as  probable. 

It  is  to  be  understood  that  the  nervous  and  digestive  systems  of 
the  child  are  in  a  developmental  condition,  and  therefore  in  unstable 
physiological  equilibrium,  so  that  any  added  physiological  work,  such 
as  unusual  growth  or  dentition,  may  be  more  than  the  organism 
can  endure  without  a  definite  loss  of  general  vital  potential.  This 
may  be  further  complicated  by  hereditary  defects  of  tissue,  such  as 
neurotic,  degenerative,  or  syphilitic  taint,  or  conditions  of  hygiene  or 
feeding  tending  to  lower  the  health  standard. 

Ottofv  offers  the  following  report  by  the  Bureau  of  Health  of 
Manila,  of  3250  deaths  before  twelve  months  of  age: 

Before  completing  one  month 647 

During  second  anrl  third  months 302 

Various  causes  not  dental 959 

Four  to  twelve  months  due  to  convulsions  and  eclampsia    ....  1342 

Total 3250 

Showing  a  large  number  of  deaths  due  to  causes  in  which  dentition 
may  have  been  a  determining  or  complicating  factor. 

Dr.  William  P.  Spratley,  medical  superintendent  of  an  institution  for 
epileptics,  states  it  as  his  opinion  that  pathological  first  and  second 
dentition  is  a  determining  cause  of  epilepsy  in  children  having 
neuropathic  taint  in  that  direction.^ 

Symptoms. — The  symptoms  of  pathological  dentition  are  both  local 
and  general. 

Local  Symptoms. — The  local  symptoms  are  usually  those  of  inflam- 
mation, red  and  .swollen  gum  ti.ssue  at  times  assuming  a  dusky  hue. 
The   gums    may    be   white,  often   glistening,  indicating   their   tense 

»  Dental  Cosmos.  1905. 


188  DENTITION 

stretching  over  the  crowns.  In  the  gum  over  the  erupting  tooth 
there  may  exist  a  vesicular  enlargement  containing  fluid. ^  Evidence  of 
local  irritability  is  given  by  the  fact  that  the  child  resists  the  touching  of 
the  gums,  seizes  the  breast  or  bottle  nipple  and  immediately  releases  it. 

The  readiness  with  which  the  child  will  take  cold  substances,  ice 
or  ice-water,  is  notable  and  self -explainable.  Alternate,  excessive  flow 
of  saliva  and  oral  dryness  is  present. 

In  the  more  marked  cases  of  local  disturbance  evidences  of  bacterial 
infection  of  the  mucous  membrane  of  the  mouth  may  make  their  ap- 
pearance, such  as  ulcerative  stomatitis.  While,  as  a  rule,  the  breaking 
down  and  ulceration  of  the  tissue  are  confined  to  the  parts  overlying 
the  erupting  teeth,  a  general  stomatitis  or  widely  scattered  patches 
of  ulceration  may  make  their  appearance.  The  localized  condition 
has  been  called  odontitis  infantum. 

General  Symptoms. — The  general  symptoms  may  be  differentiated 
into  mild  and  severe. 

The  mild  symptoms  are  such  as  are  attendant  upon  severe  and 
painful  inflammations  about  the  face  at  almost  any  age;  thus  anorexia, 
fretfulness,  anger,  restlessness,'  sleeplessness,  thirst,  mild  fever,  and 
evident  desire  for  the  upright  position  occur.  The  pain  is  at  times 
paroxysmal,  but  may  become  continuous. 

These  symptoms  subside  upon  the  eruption  of  the  tooth  or  lancing, 
though  erupting  cuspifis,  Ijound  by  a  ring  of  tense  gum  tissue  or  by 
adjoining  teeth,  may  continue  the  irritation  even  when  apparently 
erupted  (Fig.  138,  C). 

The  more  severe  general  symptoms  are  such  as  are  brought  about 
by  reflex  neuroses. 

The  roots  of  the  fifth  cranial  nerves  supplied  to  the  teeth  are  in 
intimate  relation  with  the  roots  of  the  seventh,  ninth,  and  tenth  cranial 
nerves  in  the  floor  of  the  fourth  ventricle,  as  well  as  with  other  cranial 
nerves.  It  may  be  argued  upon  a  jyrinri  grounds  that  irritation  of  the 
peripheral  ends  of  the  fifth  in  the  pulp  tissue  may  therefore  readily 
produce  neurotic  results  in  the  brain,  salivary  glands,  skin,  lungs  or 
larynx,  intestinal  canal,  or  muscles  of  the  face  or  extremities. 

Taking  the  intestinal  canal  as  tlic  most  complicated  example,  we 
find  the  following  (hita:  The  stomach  and  intestines  are  under  the 
influence  of  the  pneumogastric  nerve,  which  s(Mids  to  its  muscular  coats 
))oth  stimulant  and  inhibitory  fillers.  Tjikewise,  it  sends  viisoinoter 
fillers  to  the  intestines,  division  of  which  leads  to  inhil)iti()n  of  the 

1  Tomes,  SyHlcin  of  Ucndil  Surgery. 


PATHOLOGICAL  FIRST  DEXTITIOX  189 

muscular  fibers  of  the  vessels  and  leads  to  vasodilatation  and  a  threat 
inerease  of  very  watery  sueeu.s  enterietis.' 

Intestinal  Disturbances. — That  intestinal  disturbances  may  arise 
independently  of  teething  is  self-evident.  They  are  most  liable  to  so 
occur  during  the  very  period  during  which  teething  may  be  supposed 
to  act  as  a  primary  cause  of  intestinal  troubl(\s;  hence  differentiation 
becomes  important. 

That  the  conditions  may  be  associated  is  also  evident.  As  a  rule, 
intestinal  disturbances  arise  from  im])roper  feeding,  the  food  acting  as 
an  indigestible  irritant  to  the  stomach  and  intestines.  Even  an  exces- 
sive quantity  of  good  breast  or  bottle  milk  may,  if  not  regurgitated, 
act  as  an  intestinal  irritant.  The  milk  of  an  excited,  exhausted,  or 
debauched  nurse  may  also  act  deleteriously.  Fermentation  due  to 
bacteria  ensues,  and  diarrhea  and  colic  are  a  natural  result. 

Musser"  attributes  these  cases  to  development  of  the  Bacillus  coli 
communis  and  Bacterium  lactis  aeriformis  existing  harmlessly  in  the 
normal  intestine,  but  developing  under  the  abnormal  conditions. 

This  occurring  in  warm  weather  when  the  child  suffers  from 
intense  heat  has  a  very  debilitating  if  not  fatal  result. 

The  condition  may  be  viewed  as  an  infective  diarrhea  following  a 
vasomotor  disturbance  of  the  intestinal  walls  set  up  by  reflexes  pri- 
marily caused  by  the  indigestible  food.  The  vital  resistance  is 
lowered  by  the  disturbed  alimentation  and  the  pain. 

A  similar  train  of  circumstances  may  be  caused  by  teething. 
Peripheral  irritation  of  terminals  of  the  fifth  nerve  in  the  pulp  may, 
through  the  tenth  nerve,  cause  a  reflex  vasomotor  dilatation  in  the 
walls  of  the  intestines — /.  e.,  hyper(>mia,  a  condition  which  favors 
bacterial  invasion.  Intestinal  digestion  is  disordered,  the  vital 
resistance  lowered,  and  an  intVx'tion  ordinarily  resisted  occurs. 

Diarrhea  may  follow.  In  either  case  alimentation  is  interfered  with 
and  the  general  nutrition  suffers.  The  child  is  debilitated  by  lack  of 
nutrition;  moreover,  toxic  substances  are  generated  in  the  intestine 
which  cause  a  toxemia,  to  which  many  of  the  general  symptoms 
may  be  attributol,  such  as  fever,  meningitis,  stupor,  coma,  and  death. 
The  general  debility  also  further  interferes  with  the  process  of  dentition. 

Diagnosis. — A  diarrhea  due  to  imj)roper  feeding  would  not  be 
preceded  by  symptoms  of  pathological  dentition,  would  have  a  history 
of  improper  feeding,  and  possibly  of  unhygienic  conditions,  such  as 
unsterilized  milk  or  milk  bottles,  filthy  surroundings,  etc.     There  is 

',  Halliburton,  Kirkes'  Physiology,  189G,  p.  68-i.  =■  Medical  Diagnosis. 


190  DENTITION 

a  catarrhal  diarrhea  accompanied  by  vomiting  and  constant  acid, 
watery  stools.  The  stools  may  have  a  chopped-spinach  character. 
There  is  colic  due  to  collections  of  gas. 

Such  an  infective  diarrhea  may  readily  follow  the  reflex  and  debil- 
itating effects  of  pathological  dentition,  as  shown  above. 

AMiite^  has  noted  that  a  choleraic  diarrhea  may  accompany  and  be 
a  sign  of  pathological  dentition.  Barrett^  states  that  a  diarrhea  due 
to  dentition  will  probably  be  followed  by  constipation. 

A  symptomatic  diarrhea  will,  as  a  rule,  be  accompanied  by  signs 
of  pathological  dentition  at  points  in  the  jaws  at  which  teeth  should 
be  in  process  of  eruption. 

Nervous  Disturbances. — Disorders  referable  to  the  central 
nervous  system  are  the  most  alarming  and  are  those  indicating  the 
higher  grades  of  severity  of  irritation. 

The  milder  forms  of  these  are  faint  muscular  twitchings  and  evi- 
dences of  slight  cerebral  disturbance. 

Either  of  these  may  be  the  result  of  poisons  absorbed  from  the 
alimentary  canal  during  the  course  of  intestinal  fermentation,  but  as 
cases  of  even  convulsions  have  occurred  without  other  cause  than 
teething  apparent  and  been  relieved  by  lancing  alone,  the  possibility 
of  direct  connection  between  teething  and  central  nervous  disturbance 
must  be  admitted. 

A  distressing  symptom,  not  easy  to  elicit  on  account  of  the  age  of 
the  patient,  is  headache.  The  child  is  sleepless,  and  cries  without 
apparent  cause;  it  becomes  quiet,  partially  from  exhaustion,  and  after 
a  period  again  commences  sobbing.  The  indication  of  central  dis- 
turbance may  at  times  be  noted  in  the  contracted  pupils  of  the  eyes 
and  in  throbbing  arteries.  The  usual  treatment,  the  administration 
of  chloral  hydrate  and  potassium  bromide,  with  cold  applications  to 
the  head,  furnishes  relief  which  is  frequently  not  complete  without 
attention  to  the  dental  organs. 

In  the  more  severe  and  dangerous  cases  the  evidences  of  disorder 
of  the  central  nervous  system  become  unmistakable.  These  appear 
as  clonic  convulsions  or  symptomatic  eclampsia,  \^^lile  it  is  pro})able 
in  many  cases  that  reflex  irritation  from  the  process  of  dentition  in 
itself  is  but  a  secondary  cause  of  convulsions,  yet  evidence  is  sufficient 
to  warrant  its  being  regarded  as  a  determining  factor.  In  very  many 
cases  teething  convulsions  appear  to  indicate  a  neurotic  family  taint, 
and  eclampsia  may  attend  many  disorders  in  children  of  this  type, 

•  American  System  of  Dentistry.  ^  Oral  Pathology  and  Practice. 


PATHOLOGICAL  FIRST  DENTITIOX  191 

notably  the  mechanical  and  chemical  irritation  induced  by  the 
presence  of  large  masses  of  indigestible  foofl  in  the  intestines. 

So-called  teething  convulsions  occur  usually  at  a  time  when  several 
teeth  are  in  process  of  eruption.  The  onset  of  the  convulsion  is 
rarely,  although  apparently  often,  sudden.  If  the  child  be  closely 
observed,  it  is  noted  that  a  period  of  cerebral  disturbance — fretful 
crying,  evidences  of  headache,  sleeplessness,  etc. — is  followed  by  a 
period  of  dulness  and  somnolence,  or  the  child  may  lie  with  eyes 
half  open.  Twitching  of  one  or  more  groups  of  muscles  may  be 
observed;  the  orbicularis  oris  and  other  muscles  of  the  lips,  and  the 
muscles  of  the  eye,  notably  the  superior  and  internal  recti,  may  con- 
tract spasmodically.  A  common  muscular  spasm  ushering  in  convul- 
sions is  that  of  the  adductor  muscles  of  the  thumb;  the  thumbs  are 
drawn  toward  the  palms  of  the  hands.  The  adductor  muscles  of 
the  feet  contracting,  the  feet  are  drawn  inward.  This  period  may 
be  ushered  in  by  a  sharp  cry,  the  eyes  roll  upward  with  the  lids 
half  open,  and  consciousness  is  lost.  The  symptoms  may  disappear, 
the  child  awakening  dazed  and  fretful;  or  it  may  sink  into  sleep. 
Unless  the  source  of  irritation  be  removed,  or  active  therapeutic 
measures  be  instituted,  the  eclampsia  may  return  and  in  severe  cases 
be  the  precursor  of  death. 

Infantile  paralysis  of  a  grouj)  of  muscles  or  even  a  single  muscle 
has  been  recorded,  lasting  from  a  few  days  to  months,  appearing  with 
dentition  and  disa])peanng  after  it.  In  some  cases  it  persists  for 
life.'     Strabismus,  if  produced,  may  also  persist. 

Skin  Disorders. — It  is  so  common  as  to  be  almost  termed  the  rule 
to  find  that  when  there  are  intestinal  symptoms  there  are  eruptions 
observable  on  the  skin.  The  mildest  form  of  these  is  an  herpetic  erup- 
tion about  the  mouth;  in  other  cases  papular  and  vesicular  eruptions 
are  observed  upon  the  skin  of  the  body  and  limbs. 

Occurring  within  the  mouth  infection  may  be  added  and  ulcerative 
stomatitis  may  occur  upon  the  gums,  tongue,  lips,  or  inside  of  the 
cheek. 

Pulmonary  Symptoms. — Pulmonary  irritation  may  be  expressed  in 
laryngeal  cough  attending  the  eruption  of  teeth  and  flisappcaring 
thereafter. 

Treatment  of  Pathological  First  Dentition. — This  may  be  divided  into 
prophylactic  and  remedial.  The  prophylactic  measures  include  care 
as  to  pasteurization  of    milk  or  modified  milk  diet,  sterilization  of 

'  White,  ••Vmerican  System  of  Dentistry. 


192  DENTITION 

bottles,  bottle  nipples  and  rings,  the  prevention  of  the  introduction  of 
unclean  fingers  into  the  mouth  of  the  child,  and  the  antiseptic  care 
of  its  mouth  by  frequent  washings  with  a  saturated  solution  of  boric 
acid  in  water.  This  last  may  be  applied  to  the  mouth  on  a  soft,  linen 
rag  wrapped  on  the  forefinger.  These  measures,  together  with  the 
proper  feeding,  ventilation,  and  care  as  to  clothing,  which  should 
give  comfort  and  not  be  in  any  way  irritating,  tend  to  prevent  intestinal 
fermentation  and  to  reduce  the  general  irritability  of  the  infant. 

Remedial  Measures. — To  reduce  local  hyperemia  of  the  gum 
above  an  erupting  tooth  a  common  domestic  measure  is  valuable,  viz., 
a  small  block  of  ice  is  placed  in  a  corner  of  a  clean  napkin,  and  con- 
fined in  place  by  a  thread;  the  infant  places  it  in  its  mouth  at  pleasure 
if  old  enough,  or  the  nurse  permits  the  child  to  bite  upon  it.  The 
mechanical  effect  of  biting  upon  a  hard  substance  has  added  to  it  a 
degree  of  cold  which  lessens  the  local  vascular  engorgement. 

Any  severe  local  irritation  about  erupting  teeth  should  be  relieved 
by  thorough  lancing  of  the  gum.  It  is  irrational  that  the  child  should 
be  permitted  to  suffer  from  local  irritation  which  may  develop  into 
more  serious  complications. 

This  operation  is  performed  by  dividing  the  gum  lineally  over  the 
incisors  and  cuspids  before  eruption,  crucially  over  the  cuspids  after 
eruption  of  the  cusps  only,  crucially  over  the  upper  first  molar,  and 
with  an  X  incision  over  the  upper  second  and  lower  first  and  second 
molars  (Fig.  138). 

For  severe  cases  Flagg  advised  the  removal  of  a  block  of  gum 
from  over  a  molar.  A  cut  is  made  parallel  with  the  lingual  side 
of  the  crown,  a  second  parallel  with  the  buccal  side,  a  third  parallel 
with  the  mesial  side.  A  tenaculum  is  thrust  into  the  block  of  gum, 
which  is  drawn  tense  and  then  divided  at  the  distal  portion,  preferably 
with  a  pair  of  curved  gum  scissors.  Lacking  these  latter,  the  bistoury 
may  be  used. 

The  cut  over  the  upper  incisors  should,  if  possible,  be  made  a 
little  to  the  outside  of  the  cutting  edge,  that  for  the  lower  to  the 
inside,  in  order  that  their  crowns  may  take  a  proper  direction  toward 
occlusion. 

The  instrument  to  be  used  is  a  sharp-pointed  bistoury,  as  it  pene- 
trates well  and  permits  a  free  draw  cut.  It  is  to  be  wrapped  with 
tape  or  a  strip  of  linen  cloth  until  only  a  half  inch  of  the  point  is 
exposed.  This  precaution  prevents  accidental  wounds.  The  child 
must  be  securely  held  by  an  assistant  the  least  sympathetic  available. 


PATHOLOGICAL  FIRST  DEXTITION  193 

Flagg's  method  was  to  place  the  child  upon  its  back  across  the  lap 
of  the  assistant,  who,  in  one  position,  places  his  left  hand  over  the 
child's  eyes,  securing  the  head;  his  right  hand  secures  the  hands  upon 
the  abdomen,  while  the  legs  are  held  against  his  body  by  the  right 
arm.  The  position  may  be  exactly  reversed.  The  feet  should  be 
placed  toward  the  light  for  the  upper  jaw,  the  reverse  for  the  lower 
jaw.  In  another  position  the  child  sits  upon  one  thigh  of  the  assistant, 
the  back  of  the  head  resting  upon  the  chest,  and  the  hand  of  that  side 
(usually  the  right)  pressed  upon  the  child's  forehead  to  hold  the  head 
firmly.  The  other  hand  and  forearm  hold  the  child's  arms  and  legs 
firmly. 

The  operator  encloses  the  gum  about  the  part  to  be  cut  with  the 
thumb  and  forefinger  of  the  left  hand,  so  that  the  bistoury  cannot  slip 
and  cut  lip,  cheek,  or  tongue.  Incision  over  the  erupting  tooth 
should  be  made  until  the  knife-blade  is  felt  to  touch  the  enamel 
surface.  The  operation  of  scarifying  the  gunis,  making  merely  a  few 
scratches  to  relieve  engorged  vessels,  is  but  temporizing  with  the  con- 
dition; the  cut  should  be  of  sufficient  extent  to  entirely  remove  tension 
from  above  the  tooth.  The  little  finger  of  the  right  hand  may  rest 
upon  the  chin  of  the  child  as  an  additional  guard. 

If  the  child  bite,  a  cork  with  a  string  attached  for  safety  may  be 
used  as  a  prop. 

More  or  less  bleeding  follows  upon  the  operation,  and,  as  a  rule, 
ceases  spontaneously.  A  short  period  of  bleeding  is  desirable,  so  that 
vascular  engorgement  may  be  reduced.  Suckling  by  the  breast  or 
bottle  usually  serves  to  check  the  bleeding;  the  tissues  about  the  cut 
surfaces  are  compressed  by  tongue  and  lips  during  suckling,  and 
bleeding  ceases.  In  the  event  of  the  bleeding  continuing,  the  mouth 
should  be  carefully  examined,  and  a  piece  of  ice  in  a  napkin  may  be 
given  the  child  to  suck.  The  child  may  swallow  the  blood  and  later 
regurgitate  it.  Obstinate  bleeding  may  require  the  use  of  styptics, 
but  these  should  be  of  a  character  to  cause  only  coagulation  of  the 
blood,  not  the  destruction  of  tissue.  A  little  powdered  tannin  laid 
upon  the  cut  acts  promptly,  as  does  also  a  small  amount  of  powdered 
alum.  In  some  cases  the  internal  treatment  may  be  necessary. 
(See  Hemophilia.) 

Death  has  occurred  from  hemorrhage  due  to  lancing  in  cases  of 

presumably  hemorrhagic  diathesis;  so  that  inquiry  as  to  family  history 

would  be  a  wise  precaution.     Obtaining  such  a  history,  the  gravity  of 

the  symptoms  alone  warrant  the  operation.     In  the  absence  of  sr.ch 

13 


194  DENTITION 

a  history  the  operation  is  to  be  held  as  trivial.  If  it  occurs  it  should 
be  treated  as  indicated  on  p.  113. 

The  operation  of  lancing  is  warranted  even  when  the  gum  may 
be  likely  to  heal  over  the  tooth  by  formation  of  cicatricial  tissue, 
provided  symptoms  demand  it.  It  is  contra-indicated  in  diphtheria 
and  erysipelas  owing  to  the  danger  of  infection. 

Shock  has  occurred  in  long-continued  debilitated  cases,  and  if 
feared  a  trifle  of  brandy  in  water  may  be  given  previous  to  the  opera- 
tion. 

It  is  within  the  knowledge  of  the  writer  that  a  physician  has  refused 
to  lance  the  gums  in  a  case  diagnosticated  as  cerebral  meningitis, 
even  when  death  was  prognosticated  and  though  the  child  was  at 
an  age  rendering  pathological  dentition  possible,  and  in  spite  of  a 
history  of  pathological  dentition  in  a  previous  child  at  the  same  age. 
J.  Lewis  Smith^  concedes  the  similarity  of  occasional  symptoms  of 
pathological  dentition  and  cerebral  meningitis,  so  that  the  above 
therapy  was  foolish,  to  say  the  least,  and  especially  so  in  view  of  the 
probable  death,  which  did  occur.  In  many  desperate  cases  lancing 
has  effected  marvellously  rapid  recoveries  aided  by  judicious  handling 
of  the  accessory  symptoms,  even  though  all  hope  from  ordinary 
therapy  had  been  abandoned. 

Treatment  of  Stomatitis. — Should  general  stomatitis,  with  or 
without  stomatitis  ulcerosa,  make  its  appearance,  the  mouth  is  to  be 
promptly  and  freely  sprayed  with  a  3  per  cent,  solution  of  hydrogen 
dioxide,  followed  by  a  spray  of  potassic  chlorate  (gr.  xx-5j),  which 
usually  affords  prompt  relief.  Should  the  spots  of  ulceration  not 
disappear  promptly,  the  mouth  and  tissues  about  the  ulcer  are  to  be 
guarded  by  soft  linen  napkins;  each  ulcer  is  dried  and  touched  with 
carbolic  acid,  full  strength.  The  spraying  is  to  be  repeated  at  intervals 
of  three  hours  during  the  waking  period. 

Treatment  of  Skin  Eruptions. — The  eruptions  which  appear 
upon  the  skin  during  dentition  may  be  a  source  of  annoyance  to  the 
child  by  causing  itching.  As  a  rule,  measures  directed  toward  a 
regulation  of  the  intestinal  functions  cause  a  disappearance  of  the 
skin  affections.  If  the  eruption  be  widespread  and  cause  much  itching, 
a  wash  of  phenol-sodique  diluted  to  one-third  with  water  usually 
affords  relief.  If  the  surfaces  be  then  dried  and  talc  powder  dusted 
over  them  the  condition  is  much  alleviated.  About  the  mouth  and 
over  excoriated  surfaces  an  ointment  of  zinc  oxide  is  useful. 

1  Diseases  of  Cliiidren. 


PATHOLOGICAL  FIRST  DENTITION  195 

Treatment  of  Intestinal  Symptoms.^ — Tlio  fermentative  material 
in  the  bowel,  together  with  the  great  mass  of  bacteria  present,  should 
be  removed  by  the  use  of  a  cathartic.  It  is  indicated  in  both  con- 
stipation and  diarrhea.  Castor  oil  serves  well,  and  is  readily  taken 
by  children.  To  lessen  the  irritation  of  the  bowel  laufianum  and 
powdered  acacia  may  be  adderl. 

The  following  formula  may  safely  be  used  even  at  six  months  of  age: 

I^. — Tincturae  opii Ktt.  x 

Olei  ricini f3J''s 

Pulveris  acaciiE 5 1 J 

Saccharin gr.  ij 

Aqu£E  cinnamomi  q.  s.  ad      f3''J — M. 

Sig. — Shake  the  bottle,  and  give  one  teaspoonful  each  two  hours  if  needed. 

For  an  additional  six  months  of  age  ten  drops  more  of  laudanum 
may  be  added  to  the  general  formula.  In  mild  cases  olive  oil  in  half- 
teaspoonful  doses  may  be  substituted. 

Following  catharsis,  antacid  sedative  astringents  and  intestinal 
antiseptics  are  indicated : 

I^.— Salol 3J 

Bismuthi  subnit 3ij 

Mistura;  cretaj ad  f5'ij- — M- 

Sig. — One  teaspoonful  everj'  four  hours.     (Diddle.) 

I^. — Tinctura;  opii gtt.  xvj 

Bismuthi  subnit S'j 

Misturae  cretse SJss 

Syr.  simp SJss — M. 

Sig. — Shake  well,  and  give  in  teaspoonful  doses  every  four  hours.     (Barrett.) 

The  virtues  of  both  formula;  may  be  obtained  by  including  the 
laudanum  (gtt.  xii)  with  the  salol  formula. 

Listerine  in  10-drop  doses,  in  water,  every  three  hours,  serves  as  an 
intestinal  antiseptic. 

The  gums  are,  of  course,  to  be  lanced  at  the  outset  if  the  diarrhea 
be  due  to  pathological  dentition.  Following  the  intestinal  antisepsis 
the  general  debility  and  possible  intestinal  toxemia  (see  page  139)  is 
to  have  careful  attention,  and  the  child's  food  is  to  be  properly  adjusted 
to  its  needs. 

J.  Lewis  Smith  claims  that  upon  the  following  diet  ill-'conditioned 
children  under  his  care  in  the  hospital  escape  summer  diarrhea  and 
thrive;  the  diet  is  therefore  here  introduced. 

For  children  not  nourished  on  breast  milk  of  good  quality,  and  those 
over  three  months,  he  recommends  the  following  substitutes: 

1.  Heat  barley  flour  in  a  double  boiler,  the  water  in  the  outer  vessel 
to  be  kept  boiling  for  five  to  seven  days  to  Inirst  the  starch  granules 
(Robinson's  prepared  barley  flour  can  be  bought). 


196  DENTITION 

2.  Take  of  this  flour  one  tablespoonful,  add  25  or  30  table- 
spoonfuls  of  boiling  water  and  boil  and  mix  for  five  minutes.  Cool 
to  blood  heat,  add  1  dram  of  diastase  to  change  the  starch  to  dextrin 
and  maltose.  Forbes'  diastase  or  Taka-diastase  can  be  bought.  Of 
the  latter  1  grain  will  change  150  grains  of  starch  to  sugar. 

Pasteurize  milk  by  heating  for  twenty  minutes  to  160''  F.  Cool 
quickly  on  ice  and  let  the  cream  separate.  To  two  and  one-half 
ounces  of  the  upper  half  add  a  little  peptogenic  mild  powder  (Fair- 
child's)  to  peptonize  it.  He  feeds  the  infant  nine  or  ten  times  at 
two-hour  intervals,  administering  the  peptonized  milk  mixed  with 
three  and  one-half  ounces  of  the  dextrinized  gruel.  Before  feeding 
administer  a  few  drops  of  a  digestive  ferment. 

For  use  in  emergency  he  recommends  two  heaped  teaspoonfuls 
of  condensed  milk  to  fifteen  teaspoonfuls  of  boiled  water,  as 
equivalent  to  seventeen  teaspoonfuls   of  ordinary  milk. 

He  gives  the  following  table  of  quantities  of  food  required  by 
infants;  either  breast  or  modified  cows'  milk  to  be  used. 


At  each  feeding. 

During  the  first  week 1  ounce. 

At  the  third  week I5  ounces. 

At  the  sixth  week 2  " 

At  the  third  month   .......  3  " 

At  the  fourth  month 4  " 

At  the  sixth  month 6  " 

At  the  tenth  to  twelflh  montli        ...  8  " 


White,  following  Starr,  gives  the  following  schedule  of  the  diet  of  a 
hand-fed  infant  from  birth  upward,^  which  will  serve  as  a  suggestive 
and  useful  guide: 

Diet  durinf/  the  First  Week. 

Creiini foiij 

Sugar  of  milk gr  xv 

Whey fSss,  fSiJ 

Water f5ss,  fSiJ- 

This  portion  to  be  given  every  two  hmirs  fioni  5  a.m.  to  11  f.M.,  and  in  .some  instances 
once  or  twice  during  the  niglit. 

Diet  jrom  the  Second  to  the  Fifth  Week. 

Milk f5«« 

Cream f5i.i 

Sugar  of  milk gr.  xv 

Water fSJ. 

This  r)ortion  to  he  given  every  two  hourw  from  .^  a.m.  to  1  1  p.m. 

'  Disea.ses  of  the  Digestive  Organs  in  Infancy  and  (Iliiidliood,  by  Louis  Starr,  M.D. 


Number 

of 

Total  daily 

daily  feedings. 

quantity. 

10 

10  ounces. 

10 

15       " 

8 

16        " 

8 

24 

7 

28       " 

6 

36 

PATHOLOGICAL  FIRST  DENTITION  197 

Diet  from  the  Fift/i  Week  to  the  End  of  the  Second  Month. 

Milk f3J.  foij 

Cream f3ss 

Sugar  of  milk Kr.  xxx 

Water f3J.  foij- 

This  portion  to  he  given  every  two  hours. 

Diet  duritig  the   Third  Month. 

Milk          fSiiss 

Cream f5ss 

Sugar  of  Milk oj 

Water f5J. 

This  portion  to  be  given  every  two  and  a  half  hours. 

Diet  during  the  Fourth  anil  Fifth  .Months. 

Milk f^iiiss 

Cream fSss 

Sugar  vl  milk oj 

Water fSJ- 

This  portion  to  be  given  every  three  hours. 

Diet  during  the  Sixth  Month. 

Milk fjivss 

Cream f5ss 

Sugar  of  milk 5J 

Water f5J- 

This  portion  to  be  given  four  times  daily. 

Two  other  meals — morning  and  mid-day — may  be  as  follows: 

Milk fSivss 

Cream fjss 

Mellin's  Food oj 

Hot  water f  5J. 

Dissolve  the  Mellin's  Food  in  the  hot  water,  and  add,  with  stirring,  to  the  previously  mixed 
milk  and  cream. 

In  the  seventh  month  the  Mellin's  Food  may  be  increased  to  two 
teaspoonfuls  and  given  three  times  daily. 

Throughout  the  eighth  and  ninth  months  five  meals  a  day  will  be 
sufficient — at  7  and  10.30  a.m.,  2,  G,  and  10  p.m. 

Milk f3viss 

Cream f3ss 

Sugar  of  milk 5i 

Water f3j. 

This  |)ortion  for  the  first  and  last  meals. 

For  tht>  other  three  meals  1  tabic.spoonful  of  ^Mellin's  Food  may  be 
added,  or  1  teaspoonful  of  "Hour-ball"  may  be  given  twice  daily 

instead  of  the  Mellin's  Food — say  at  the  second  and  fourth  meals. 

Diet  for  the  Tenth  and  Eleventh  Months. 

First  meal,  7  a.m.: 

Milk f3viiiss 

Cream fSss 

Mellin's  Food 5ss 

(Or  "flour  ball"  or  barley  jelly 5ij) 

Water fSJ. 

To  be  used  only  when  Mellin's  Food  is  emi)loyed. 


198  DENTITION 

Second  meal,  10.30  a.m.  :    Eight  ounces  of  warm  milk. 

Third  meal,  2  p.m.:  The  yolk  of  an  egg  lightly  boiled  with  stale 
bread  crumbs. 

Fourth  meal,  6  p.m.  :  Same  as  first. 

Fifth  meal,  10  p.m:  Same  as  second. 

On  alternate  days  the  third  meal  may  consist  of  1  teacupful  (f  §vj) 
of  beef-tea  containing  a  few  stale  bread  crumbs. 

Beef -tea  for  an  infant  is  made  in  the  following  way :  One-half  pound 
of  fresh  rump  steak,  free  from  fat,  is  cut  into  small  pieces  and  put  with 
1  pint  of  cold  water  into  a  covered  tin  saucepan.  This  must  stand 
by  the  side  of  the  fire  for  four  hours,  then  be  allowed  to  simmer 
gently  (never  boil)  for  two  hours,  and,  finally,  be  thoroughly  skimmed 
to  remove  all  grease. 

A  further  variation  can  be  made  by  occasionally  using  mutton, 
chicken,  or  veal  broths  instead  of  beef -tea. 


Diet  from  the   Twelfth  to  the  Eighteenth  Month 
{Five  Meals  a  Day). 

First  meal,  7  a.m.:  A  slice  of  stale  bread  broken  and  soaked  in  a 
breakfastcupful  (f§viij)  of  new  milk. 

Second  meal,  10  a.m.:  A  teacupful  of  milk  (f^vj)  with  a  soda  bis- 
cuit or  thin  slice  of  buttered  bread. 

Third  meal,  2  p.m.:  A  teacupful  of  beef -tea  (f§vj)  with  a  slice  of 
bread,  1  good  tablespoonful  of  rice,  and  milk  pudding. 

Fourth  meal,  6  p.m.  :  Same  as  first. 

Fifth  meal,  10  p.m.  :  One  tablespoonful  of  Mellin's  Food  with  1 
breakfastcupful  of  milk. 

To  alternate  with  this : 

First  meal,  7  a.m.  :  The  yolk  of  one  egg  slightly  boiled  with  bread 
crumbs;  1  teacupful  of  new  milk. 

Second  meal,  10  a.m.:  A  teacupful  of  milk  with  a  thin  slice  of 
buttered  bread. 

Third  meal,  2  p.m.  :  A  mashed  boiled  potato  moistened  with  4 
tablespoonfuls  of  beef -tea;  2  good  tablespoonfuls  of  junket. 

Fourth  meal,  6  p.m.:  A  breakfastcupful  of  new  milk  with  a  slice 
of  bread  broken  up  and  soaked  in  it. 

Fifth  meal,  10  p.m.:  Same  as  second. 

The  fifth  meal  is  often  unnecessary,  and  sleep  should  not  be  dis- 
turbed for  it.     At  the  same  time,  should  the  child  awake  an  hour  or 


PATHOLOGICAL  FIRST  DEXTITIOX  199 

more  before  the  first  meal  time,  lie  should  break  his  fast  upon  a  euj) 
of  warm  milk,  and  not  be  allowed  to  go  hungry  until  the  set  breakfast 
hour. 


Diet  from  Eighteen  Months  to  the  End  of  Tiro  and  One-half 
Years   (Four  Meals  a  Day). 

First  meal,  7  a.m.:  A  breakfastcupfnl  of  new  milk;  the  yolk  of 
one  egg  lighdy  l)oiled;  two  thin  slices  of  bread  and  butter. 

Second  meal,  11  a.m.  :  A  teacupful  of  milk  with  soda  biscuit. 

Third  meal,  2  p.m.:  A  breakfastcupfnl  of  beef-tea,  mutton  or 
chicken  broth,  a  thin  slice  of  stale  bread,  a  saucer  of  rice,  and  milk 
pudding. 

Fourth  meal,  6.30  p.m.  :  A  breakfastcupfnl  of  milk  with  bread  and 
butter. 

On  alternate  days: 

First  meal,  7  a.m.  :  2  tablespoonfuls  of  thoroughly  cooked  oat- 
meal or  wheaten  grits,  with  sugar  and  cream;  1  teacupful  of  new 
milk. 

Second  meal,  11  a.m.  :  A  teacupful  of  milk  with  a  slice  of  bread  and 
butter. 

Third  meal,  2  p.m.:  1  tablespoonful  of  underdone  nuitton  j)ounded 
to  a  paste;  bread  and  butter,  or  a  mashed  potato  moistened  with  good 
plain  dish  gravy;  a  saucer  of  junket. 

Fourth  meal,  6.30  p.m.:  A  breakfastcupfnl  of  milk,  a  slice  of  soft 
milk  toast,  or  a  slice  or  two  of  bread  and  butter. 

The  foregoing  schedule  must,  of  course,  be  regardeil  as  an  average. 
Many  children  can  bear  nothing  but  milk  food  up  to  the  age  of  two 
or  even  three  years,  and  provided  enough  be  taken,  no  fear  fftr  their 
nutrition  need  be  entertained.  The  rule  to  adopt  is,  if  a  child  be 
thriving  on  milk  he  is  never  to  be  forced  to  take  additional  food  merely 
because  a  certain  age  has  been  reached.  Let  the  healthy  appetite 
be  the  guide. 

The  following  is  recommended  by  Starr  as  a  modified  milk  diet, 
and  as  a  substitute  for  mother's  milk  while  weaning. 

Pasteurized  cream fS^s 

Pasteurized  milk fjiiss 

Sugar  of  milk .~ss 

Water  boiled fjj. 

Should  tliis  not  satisfy  the  infant,  increase  the  iTiKredients  (except  cream)  to  C,  8,  or 
12  ounces. 


200  DENTITION 

Hare^  recommends  the  following  diet  list  followed  in  his  hospital 
practice: 

Diet  for  a  Child  Ttuo  Years  Old. 

Breakfast,  7.30  a.m.  :  Milk.  The  lighdy  boiled  yolk  of  an  egg; 
thin  bread  and  butter  (the  bread  to  be  one-day  old). 

Lunch,  11  A.M.:  Milk.     A  thin  slice  of  bread  and  butter. 

Dinner,  1.30  p.m.:  Beef-tea  or  small  piece  of  minced  roast  beef  or 
mutton  devoid  of  grisde.  One  well-mashed  potato  moistened  with 
gravy.     Rice  and  milk. 

Supper,  6  P.M. :  Milk.     Bread  and  butter.    . 

For  drink:  Boiled  or  filtered  water. 


Diet  for  a  Child  One  Year  Old  {Five  Meals  a  Day). 

First  meal,  7  a.m.:  2  teaspoonfuls  of  grated  flour-ball  (prepared 
as  directed  below)  in  \  pint  of  milk. 

Second  meal,  10.30  a.m.  :  ^^  P"^^  of  milk  with  4  tablespoonfuls 
of  lime-water. 

Third  meal,  2  p.m.  :  The  yolk  of  one  egg  beaten  up  in  1  teacupful 
of  milk. 

Fourth  meal,  5.30  p.m.  :  Same  as  the  first. 

Fifth  meal,  11  p.m.  :  Same  as  the  second. 

Flour-ball  is  to  be  made  by  taking  one  pound  of  good  flour — 
unbolted,  if  possible — tie  it  up  very  tightly  in. a  pudding-bag;  put  it 
in  a  pot  of  boiling  water  early  in  the  morning,  and  let  it  boil  until 
bedtime,  then  take  it  out  and  let  it  dry.  In  the  morning  peel  off  the 
surface  and  throw  away  the  thin  rind  of  dough,  and  with  a  grater 
grate  down  the  hard,  dry  mass  into  a  powder.  To  use  this,  take 
from  1  to  2  teaspoonfuls  of  the  powder,  rub  it  down  until  smooth 
with  a  tablespoonful  of  cold  milk,  and  add  1  tumblerful  of  hot  milk, 
stirring  it  well  all  the  time. 

Diet  for  a  Child  from  Six  to  Twelve  Months  Old 
(  Five  Meals  a  Day). 

First  meal,  7  a.m.:  Mellin's  Food,  1  tablespoonful;  or  flour-ball 
grated,  1  or  2  teaspoonfuls  (prepared  as  directed  above);  hot  water, 

1  Practical  Therapeutics. 


PATHOLOGICAL  FIRST  DEXTITIOX  201 

4  tablespoonfiils;  warm  milk,  ('ii<)n<i;h  to  make  \  ])iiit.  Dissolve  the 
Mellin's  Food  or  rub  down  the  grated  fiour-hall  in  the  hot  water  by 
stirring,  then  add  the  milk;  mix  thoroughly. 

Second  meal,  10.30  a.m.,  and  tliird  meal,  2  i'.m.  :  A  breakfast- 
cupful  of  milk  with  4  tablespoonfuls  of  lime-water. 

Fourth  meal,  5.30  p.m.  :  Same  as  first. 

Fifth  meal,  10.30  p.m.  :  Same  as  second. 

Treatment  of  Nervous  Conditions. — If  nervous  reflexes,  great 
irritability,  or  cerebral  congestion  appear,  attention  should  be  directed 
to  the  condition  of  the  bowels  and  the  teeth. 

If  constipation  or  diarrhea  exist,  a  cathartic  is  given  and  the  gums 
are  lanced.     A  cerebral  sedative  is  to  be  prescribed. 

I^. — Chloral  hydrat gr.  ij 

Sodii  brom gr.  v 

Aquae  menthae  pip fSiJ — M. 

Sig.^Per  orem.     One  dose;  enlarge  formula  for  repetition  as  needed. 

If  convulsions  be  threatened,  the  clothing  should  be  loosened  and 
cool  applications  made  to  the  head. 

If  the  child  be  in  convulsions,  it  should  be  immersed  to  the  waist 
in  water  as  hot  as  can  be  borne,  to  which  has  been  added  2  tal)le- 
spoonfuls  of  common  mustard  flour,  and  cool  water  poured  over  its 
head,  when,  as  a  rule,  the  symptoms  promptly  subside.  Chloroform, 
which  children  endure  well,  may  be  administered. 

After  immersion  a  rectal  injection  of  1  dram  of  glycerin  or  a 
glycerin  suppository  will  usually  cause  a  free  stool.  A  cerebral 
sedative  should  be  administered. 

I^. — Chloral  hydrat gr.  ij 

Sodii  brom gr.  v 

Starch  paste 3ij — M. 

Sig. — To  be  administered  per  rectum.      (Atkinson.) 

It  is  well  also  to  administer  a  cathartic  to  unload  tiie  intestines  of 
irritating  substances  possibly  present. 

After  sleep,  if  appearances  indicating  dental  irritation  be  observed, 
gum  lancing  is  practised.  It  is  wise  that  this  operation  be  thus  deferred, 
as  convulsions  may  be  precipitated  by  the  act  of  lancing  when  the 
nervous  system  of  the  child  is  overexcited.  The  removal  of  intestinal 
irritants  by  a  cathartic  given  per  orem  is  also  in  order  before  lancing. 

It  has  been  repeatedly  noted  that  where  evidence  of  marked  cerebro- 
spinal irritation  is  present,  for  which  no  probable  source  can  be 
assigned,  and  an  examination  of  the  gums  shows  no  apparent  local 
disturbance,  yet  if  it  be  at  a  ])eriod  when  one  or  more  teeth  are  in 
process  of  eruption,  but  are  still  covered  or  bound  down  by  gum 


202  DENTITION 

tissue,  if  gum  lancing  be  practised  relief  is  immediate  and  the  lancing 
may  even  avert  a  threatened  attack  of  eclampsia.  It  is  presumed  that 
these  are  cases  of  pulp  irritation  in  which  a  failure  of  resorption  of 
tissue  in  advance  of  the  tooth  crown  has  caused  pressure  upon  the 
pulp  forming  the  root  end. 


Constitutional  States  Modifying  Dentition. 

Children  who  are  the  victims  of  hereditary  syphilis  usually  cut  their 
teeth  very  early,  the  alveolar  process  being  in  many  cases  insufficient. 
Cases  are  recorded  where  children  have  been  born  with  crowns  of  teeth 
visible  upon  the  gum,  there  being  no  evidence  of  root  formation,  the 
crowns  being  loosely  held  to  the  gum  by  fibrous  tissue.  It  is  necessary 
to  remove  these  loose  crowns  to  permit  the  infant  to  suckle.  Children 
affected  with  rachitis  have  the  process  of  eruption  much  delayed.  It  is 
seen,  therefore,  that  the  presence  of  loose  crowns  of  teeth  is  a  condition 
pointing  to,  though  by  no  means  diagnostic  of,  hereditary  syphilis. 
Long-delayed  eruption  of  teeth  should  prompt  a  search  for  further 
indications  of  rachitis.  Particularly  in  children  in  whom  a  history 
of  hereditary  syphilis  is  obtainable  the  process  of  dentition  may  be 
accompanied  by  rapid  and  frequently  widespread  breaking  down  of 
the  soft  tissues  over  and  about  erupting  teeth.  Local  measures  of 
treatment  seem  to  be  of  but  little  avail,  except  that  antiseptic  treat- 
ment undoubtedly  prevents  complications  from  extraneous  infection. 

In  children  classified  indefinitely  as  strumous,  which  may  mean  the 
children  of  syphilitic  or  tuberculous  parents,  or  those  with  no  such 
history  whose  surroundings  are  of  the  most  unhygienic  kind,  the 
process  of  dentition  may  not  only  have  an  untoward  course,  but 
phagedenic  ulcerations  may  occur.  It  is  usually  in  the  degree  of  a 
child's  debility,  either  inherited  or  acquired  through  improper  care, 
that  dentition  assumes  morbid  features.  The  treatment  of  such  cases 
must  be  directed  to  raising  the  health  standard.  As  local  therapeusis, 
no  measures  seem  more  eft'ective  than  the  sprays  of  hydrogen  dioxide 
first;  next,  potassium  chlorate,  and,  if  conditions  indicate  it,  sprays  of 
dihit(!  listerine,  which  is  stimulant,  antiseptic,  and  slightly  astringent. 

Infantile  Scurvy. — Cases  are  recorded  in  which  the  improper 
feeding  of  children  has  been  followed  by  evidences  of  scorbutus.  It 
occurs  usually  in  bottle-fed  bailies  confined  to  patent  foods,  the  nutritive 
element  being  lacking.     The  gums  become  tumid,  and  hemorrhagic 


THE  SECOND  DENTITION  203 

extravasations  occur  in  their  substance;  the  periosteum  is  stripped 
from  the  margins  of  the  alveolar  walls,  the  soft  tissues  hanging  in 
discolored,  pendulous  masses  about  and  beyond  the  teeth  if  any  be 
erupted. 

The  child  is  peevish,  listless,  and  feeble.  There  is  apparent  pain 
in  the  limbs. ^    The  urine  may  be  bloody  even  as  a  first  sign. 

The  treatment  is  largely  systemic,  and  consists  of  using  fresh  cows' 
milk  modified  to  conform  to  human  milk,  and  in  the  administration 
of  fresh  lemon  juice,  preferably  boiled,  allowed  to  settle,  and  the 
supernatant  fluid  used,"  or  orange  juice  is  also  used. 

The  mouth  should  be  sprayed  with  sedative  antiseptics,  such  as 
potassium  chlorate  in  hydrogen  dioxide  (p.  194), 


THE  SECOND   DENTITION. 

By  reference  to  Fig.  110  it  will  be  seen  that  at  six  and  one-half  years 
of  age  the  twenty  temporary  teeth  are  still  all  in  position,  and  that 
taking  their  places  in  the  line  of  the  arch  are  the  four  permanent  first 
molars,  the  roots  of  which  are  still  incomplete. 

These  molars  do  not  replace  any  temporary  teeth,  but  during  the 
"change"  support  the  jaws  with  the  assistance  of  the  temporary 
molars  until  the  permanent  incisors  are  fully  erupted,  and  with  the  aid 
of  the  incisors  until  the  bicuspids  come  into  occlusion.  Their  office 
as  jaw  props  and  organs  of  mastication  during  the  change  is,  there- 
fore, very  important.  Of  their  later  function  more  will  be  said 
farther  on. 

At  six  and  one-half  years  the  crov/ns  of  the  permanent  incisors 
lie  in  the  relations  shown  with  the  temporary  central  roots  resorbed 
and  the  lateral  root  partly  so.  Their  crowns  are  practically  complete, 
but  the  roots  are  unformed. 

The  cuspid  crown  in  its  crypt  lies  well  above  and  lingual  to  the 
unresorbed  temporary  cuspid  root.  The  roots  of  the  first  and  second 
temporary  molars,  a  trifle  resorbed  upon  the  inner  side,  embrace  the 
formed  crowns  of  the  first  and  second  bicuspids. 

In  their  crypts  back  of  the  first  molars  lie  the  forming  crowns  of 
the  second  permanent  molars.  The  third  molars  are  not  in  evidence 
in  the  illustration,  but  their  development  is  in  progress. 

It  will    be  seen  that  the  permanent  central  and  lateral    incisors 

»  Hare.  ^  Ibid. 


204  DENTITION 

replace  the  temporary  central  and  lateral  incisors,  the  permanent 
cuspid  the  temporary  cuspid,  and  the  first  and  second  bicuspids  the 
first  and  second  temporary  molars,  respectively. 

From  this  age  to  adult  age  as  previously  the  jaw  undergoes  constant 
change,  enlarges  by  constant  resorptions  and  depositions  of  bone,  and 
changes  its  contour  to  conform  to  the  changes  occurring  throughout 
the  body,  and  to  accommodate  the  permanent  teeth,  which  are  in 
general  terms  larger  and  more  numerous  than  the  temporary  teeth. 

It  may  be  said  that  the  alveolar  process  built  about  the  roots  of 
temporary  teeth  and  the  roots  of  the  temporary  teeth  are  all  resorbed 
during  the  replacement  of  the  latter,  and  that  when  the  crowns  of 
the  permanent  teeth  are  fully  erupted  new  alveolar  process  is  built 
up  about  their  roots.  Any  subsequent  change  in  the  position  of  the 
permanent  teeth  is  accompanied  by  an  alteration  in  the  alveolar 
process,  and  after  extraction  the  latter  is  resorbed,  but  upon  an  implan- 
tation (which  see)  being  done  new  process  will  form.  Its  dependence 
upon  the  teeth  is,  therefore,  evident. 

The  following  table  gives  the  approximate  ages  for  the  eruption 
of  the  permanent  teeth : 

First  molars 5J^-  7  years. 

Central  incisora 7-8 

Lateral  incisors 8-9 

First  bicuspids 10     -11 

Second  bicuspids 11     -12 

Cuspids,  the  lower  usually  preceding 12     -14 

Second  molars 12     -15 

Third  molars 16-20       " 

and  indefinitely  beyond. 

The  Process  of  Resorption  of  the  Temporary  Roots. — ^After  com- 
pletion of  formation  the  roots  of  the  temporary  teeth  remain  in  this 
state  but  a  short  time,  as  their  successors  are  ready  to  advance  to 
their  places. 

Comparing  the  ages  at  which  resorption  begins  with  the  ages  at 
which  it  is  complete  (eruption  of  permanent  tooth)  (see  Fig.  140),  it 
will  be  noted  that  approximately  three  and  one-half  years  are  required 
in  all  cases  for  the  removal  of  the  temporary  roots.  Therefore,  to 
determine  the  age  at  which  absorption  begins  deduct  three  and  one- 
half  years  from  the  date  of  eruption  of  the  corresponding  permanent 
tooth. 

At  the  time  the  permanent  tooth  begins  its  advance  it  lies  in  a 
bony  crypt  alxwe  and  lingual  to  its  predecessor,  exc(>pt  in  tlie  case 
of  the  bicuspids,  which  lie  between  the  roots  of  the  temporary  molars 
(Figs.  110  and  206). 


THE  SECOND  DEXTITIOX 


205 


Each  crypt  lias  its  own  follicle  wall  enclosing  a  permanent  tooth 
crown. 


Fig.  140 


Decalcifioation  of  the  deciduous  teetli.     The  numbers  indicate  years.     (Peirce.) 

In  the  follicular  wall  overlyino-  the  crown  appear  large  multinu- 
cleated cells  the  origin  of  which  is  unknown,  hut  which  by  some  are 
thought  to  be  transformed  osteoblasts,  by  others  leukocytes  (Figs. 
141  and  142).  The  latter  is  the  prol)- 
able  explanation,  as  analogous  cells  are 
found  about  tissues  or  foreign  bodies 
about  to  undergo  resorption  anywhere 
in  the  body.  (See  Resorption.)  In  the 
particular  situation  under  consideration 
they  are  called  odontoclasts.  The  tis- 
sue between  the  root  and  crown  has 
by  Tomes  been  given  the  name  of  the 
"absorbent  organ"  (tigs.  141  A,  and 
142).  These  giant  cells  have  a  solvent 
or  digestive  function  not  understood, 
but  which  is  competent  to  remove  both 
the  organic  and  inorganic  matter  of 
cementum  and  dentine,  and  evidences 
of  action  upon  enamel  in  other  situa- 
tions are  not  wanting.  (See  Resorp- 
tion of  Enamel.)  That  the  solvent  is 
acid  is  shown  by  the  evidence  of  de- 
calcification about  the  area  of  resorbed 
enamel  of  unerupted  erowns  of  some 

permanent  teeth.  It  is  a  curious  fact  tiiat  no  evidiMice  of  decalcifi- 
cation of  the  j^ermanent  erown  has  l)een  demonstrated  to  result 
from  the  proximity  of  the  multinucleated   eells   in  cases  of  physio- 


A- 


SIiowiiiK  tlie  relations  of  an  erupt- 
ing pennanent  tooth  to  its  deciduous 
predecessor:   A,  A,  .1,   odontiK-lasts. 


206 


DENTITION 


logical 
by  the 
These 


resorption  of  roots.  In  all  probability  the  enamel  is  protected 
presence  of  Nasmyth's  membrane,  which  is  resistant  to  acids, 
cells  are  probably  invited  by  irritation'^due  to  pressure  of  the 


Fig.  142 


Fig.  143 


The  structure  of  the  absorbent  organ,  show- 
ing multinucleated  or  giant  cells  (odontoclasts). 
(Tomes.) 


Imprisonment  of  second  temporary 
molar;  resorption  of  its  roots,  with  ab- 
sence of  second  bicuspid.  (Skiagraph 
by  Custer.) 


advancing  permanent  tooth  crown,  as  the  resorption  is  almost  always 
found  at  the  point  of  approximation  of  the  crown  with  the  root,  or, 
in  other  words,  at  the  pressure  point  (Fig.  144). 


Fig.  144 


Phases  of  resorption  of  temporary  roots.     (Skiagraph  by  Price.') 

Cases  of  resorption  of  temporary  roots  without  the  presence  of  a 
permanent  crown  are,  however,  noted  and  explained  by  Tomes 
\\\Hn\  the  ground  that  resorption  is  a  vital  act  independent  of  the  press- 
ure exerted  (Fig  143).     As  resorption  of  permanent  roots,  however,  has 


'  Items  of  Interest,  1901. 


THE  SECOND  DENTITION 


207 


Fig.  145 


often  occurred  from  pressure  of  the  crown  of  another  to(jth  and  occurs 
at  the  pressure  point  in  pliysiological  resorption,  locahzed  irritation, 
even  in  tlie  absence  of  a  permanent  crown,  must  be  credited  with  a 
hirge  influence  in  the  process.  It  is  to  be  remembered  also  that  in 
the  absence  of  the  pressure  resorption  often  does  not  occur,  at  least 
for  twenty-five  or  more  years — e.  (/.,  wlien  laterals  are  absent  and  the 
permanent  cuspids  erupt  to  the  side  of  the  deciduous 
cuspids  (Fig.  147). 

According  to  Tomes,  redeposition  of  cementum  oc- 
curs in  previously  resorbed  areas  upon  temporary  roots, 
a  fact  corresponding  with  effects  noted  in  permanent 
roots. 

Teeth  frequently  erupt  lingually  or  labially  to  their 
corresponding  temporary  teeth,  both  remaining  in  the 
mouth.  It  is  almost  invariably  the  rule  upon  extraction 
to  find  that  an  oblitjue  resorption  has  occurred,  as  is 
shown  in  the  right  upper  skiagraph  in  Fig.  144,  and  DiaKram  iiius- 
generally   a  decided  hvpervascularity  is    seen  in  the     '^ting  the  reia- 

.  '  .  tion  of  a  resorbed 

pulp  extending  upward  for  perhaps  a  quarter  of  an  inch,  temporary  root 
Doskow^  has  shown,  by  the  prompt  loss,  by  absorp-  ^'^^^^  t'ooth'^™*o 
tion,  of  a  fairly  firm  deciduous  cuspitl  crowned  to  t'le  involvement 
bnng  it  up  to  level  and  so  to  useiulness,  that  such 
an  operation  is  ina(lvisal)le  because  of  an  inherent  ten- 
dency of  a  resorbent  organ  to  become  established. 
Again,  a  permanent  tooth  undergoing  resorption  often 
remains  firm  until  suddenly  the  strain  becomes  too  great. 

As  the  root  of  the  temporary  tooth  disappears  the  pulp  continuously 
fuses  with  the  resorbent  organ,  so  that  when  the  crown  alone  remains 
the  pulp  is  still  vital  (Figs.  141  and  145).  At  times  it  seems  to  take  up 
the  resorbent  function  and  resorbs  the  crown  dentine  in  some  cases 
almost  entirely.  In  one  specimen  a  circumscribed  portion  of  the 
cementum  and  of  enamel  were  removed  by  it  at  the  point  of  junction. 
This  constituted  practically  a  case  of  perforation  by  resorption 
(Fig.  145),  The  tooth  was  at  first  thought  to  be  suffused  with 
hemoglobin,  as  it  was  of  a  pink  color.  At  times  bay-like  excavations 
in  the  crown  deiitiiu>  occur.  When  the  root  resorption  reaches  the 
point  shown  in  the  central  incisor  in  Fig.  1 10  the  temporary  tooth  is 
loosened,  moves  about,  and  annoys  the  child,  who  may  pick  it  out,  or 
it  is  removed  bv  extraction. 


part  of  the  re- 
sorbent organ. 
Resorption  of  the 
interior  of  crown 
of  a  temporary 
tooth. 


'  Dental  Cosmos,  1907. 


208 


DENTITION 


Formation  of  the  Roots  of  Permanent  Teeth. — The  extent  of  root 
development  at  any  age  is  of  great  importance  in  view  of  canal  thera- 
peutics. Incomplete  roots  present  a  mechanical  difficulty  of  sealing 
the  apex  of  the  canal.  The  size  of  the  pulp  at  the  apical  foramen 
of  such  teeth  contra-indicates  the  use  of  arsenic,  and  even  pressure 
anesthesia  is  often  unsuccessfully  applied. 

The  roots  are  developed  in  precisely  the  same  manner  as  in  the 
case  of  the  temporary  teeth,  by  the  combined  deposition  of  cementum 
by  the  osteogenetic  cells  of  the  follicularwall,  which  is  drawn  up  on  the 
root  as  a  pericementum,  and  by  the  odontoblasts  of  the  papilla,  which 
is  drawn  up  as  a  pulp  (Fig.  105). 


Fig.  146 


Absence  of  upper  left  lateral  incisor,  with  permanent  cusjjid  in  its  ijlace;    two  temporary 
cuspids  retained.      Man,  aged  iwenty-five  years. 

The  extent  of  development  of  any  of  the  permanent  teeth  may  be 
seen  at  a  glance  by  reference  to  the  valuable  table  of  Peirce  (Fig.  111). 
So  graphically  does  this  table  give  the  desired  information  that  expla- 
nation becomes  unnecessary. 

Irregularities  of  Second  Dentition. — Some  temporary  teeth  may 
be  retained  hjiig  after  a(hdt  age  is  reached.  The  teeth  most  subject 
to  this  are  the  cuspids  and  second  temporary  molars. 

In  the  case  of  the  cuspids,  the  permanent  cuspid  is  delayed  or 
takes  an  unusual  direction,  erupting  lingually  or  labially,  or  at  times 
being  directed  into  the  place  normally  occupied  by  the  lateral  incisors, 
which  are  wanting,  or  very  rarely  the  cuspid  erupts  posteriorly  to  the 


THE  SECOND  DENTITION  209 

first  bicuspid.  At  about  forty  years  of  age  the  temporary  cuspids  may 
be  lost  by  resorption  of  their  roots,  but  until  such  time  should  be 
retained  if  usefully  filling  a  space.  If  in  interference  with  proper 
alignment  or  eruption  of  the  permanent  cuspid  they  should  be  ex- 
tracted. Their  late  resorption  is  somewhat  pathological  in  character 
and  probably  due  to  or  incited  by  a  partial  resorption  of  the  root  end 
during  the  descent  of  the  permanent  cuspid. 

The  late  enforced  loss  of  the  temporary  cuspid  indicates  the  advisa- 
bility of  an  implantation  operation  (Fig.  147). 

Fig.  147 


Absence  of  upper  lateral  incisors  and  right  bicuspid.     Retention  of  temporary 
cuspids.     From  an  adult. 

The  molars  are  retained,  as  a  rule,  because  of  an  absence  of  perma- 
nent crowns  to  cause  resorption,  although  this  may  occur  without 
such  pressure  (Fig.  143).  I  have  seen  a  case  of  an  adult  lady  with 
eight  deciduous  molars  in  place.  The  question  of  the  abnormal 
development  or  absence  of  permanent  germs,  or  of  the  state  of  the 
roots  of  the  temporary  tooth  may  be  settled  by  the  x-rays  (Figs. 
143  and  148). 

The  question  of  extraction  or  retention  depends  upon  the  diagnosis. 
A  firm  temporary  tooth  should  never  be  extracted  simply  to  allow 
a  permanent  tooth  to  erupt  unless  the  presence  of  a  permanent  tooth 
in  the  jaw,  as  determined  by  skiagraph  or  other  means,  gives  reasonable 
inference  that  the  permanent  tooth  is  held  back  by  the  temporary 
14 


210 


DENTITION 


Fig.  148 


tooth.  In  most  cases  a  reasonable  delay  is  advisable.  A  patient  of 
the  editor  wore  a  plate  for  thirteen  years  because  of  the  injudicious 
extraction  of  an  upper  temporaiy  cuspid,  the  permanent  tooth  appear- 
ing at  twenty-six  years  of  age — e.  g.,  Fig.  150. 

When  the  retention  of  temporary  molars  and  cuspids  occurs,  they 
are  apt  to  occupy  an  occlusal  level  lower  than  that  of  the  permanent 

teeth  (Fig.  143).  They  may  not 
be  in  occlusion  at  all,  as  was  the 
case  with  the  eight  molars  just  re- 
ferred to.  This  proves  the  fact  that 
the  general  occlusal  level  of  the 
permanent  teeth  is  farther  from 
the  margin  of  the  alveolar  process 
than  in  the  case  of  the  temporary 
teeth.  The  length  of  the  permanent 
crowns  accounts  for  this.  In  nor- 
mal replacement,  however,  the 
occlusal  level  is  nearly  the  same 
for  the  temporary  molars  and  first  permanent  molar,  at  least  until  the 
change  is  made  by  the  eruption  of  the  bicuspid. 

The  correct  placement  of  these  first  permanent  molars  seems  to 
determine  the  correctness  of  molar  occlusion,  at  least  in  the  mesio- 
distal  relation,   though  they  may  not  occupy  their  correct  bucco- 


Retainetl    temporary   molar   with    bicuspid 
present.      (Skiagraph  by  E.  Ballard  Lodge.) 


Fig.  149 


Fig.  150 


LJ^ 


Retained  lower  temporary  molars,  bicuspid 
absent.      (Skiagraph  by  E.  Ballard  Lodge.) 


Delayed  cuspid.      (Skiagraph  by  E. 
Ballard  Lodge.) 


lingual  positions.  Any  slight  forces  disturbing  the  mesiodistal  relation 
causing  the  upper  first  molar  to  drift  anterior  to  its  correct  occlusion 
with  the  lower  molar  will  result  in  an  abnormal  relation  of  the  teeth 
to  those  anterior  to  them  and  to  their  antagonists;  either  u[)per 
protrusion   or  upper  irregularities  will  occur. 


THE  SECOND  DENTITION 


211 


If  the  reverse  occur  and  the  lower  molar  be  placed  anteriorly 
and  the  upper  be  placed  normally  or  posterior  to  its  normal  position, 
prognathism  of  the  lower  teeth  ordinarily  results.  If  placed  too  far 
posteriorly,  retrusion  of  the  lower  teeth  will  occur. 

According  to  Angle,  the  misplacement  of  the  permanent  teeth 
erupting  early  causes  their  inclined  planes  to  direct  other  teeth  from 
normal  occlusion,  or  by  permitting  contraction  of  the  space  normally 
occupied,  particidarly  in  the  lower  jaw,  permits  the  other  teeth  to 
assume  a  position  in  a  contracted  arch,  thus  again  causing  their 


Fig.  151 


Typical  occlusion.     (Cryer.) 

inclined  planes  to  cause  contraction  in  the  opposite  arch,  with  a  con- 
sequent displacement  buccolingually  of  teeth  which  would  otherwise 
normally  align  themselves  in  the  arch.  Once  establi.shed,  the  cheek 
and  lip  pressure  maintains  the  inharmony  (Fig.  156). 

Angle  divides  all  irregularities  into  three  classes,  with  divisions  and 
subdivisions: 

Class  I. — The  first  molars  are  correctly  occluded  mesiodistally, 
the  teeth  anterior  being  in  malocclusion  though  the  biscuspids  may 
be  in  correct  mesiodistal  relation. 

The  general  characteristic  of  the  class  is  that  shown  in  Fig.  152. 


212 


DENTITION 


^  Class  II. — The  lower  first  molars  occlude  distally  to  the  upper  first 
molars,  causing  retrusion  of  the  lower  jaw.  Division  I  is  character- 
ized by  distal  occlusion  on  both  sides,  the  upper  arch  is  narrowed, 
the  upper  incisors  lengthened  and  protruded.  The  upper  lip  is  short 
and  functionless,  while  the  lower  lip  is  thickened  and  rests  cushion- 
like between  the  upper  and  lower  incisors,  increasing  the  protrusion  of 
the  upper  and  the  retrusion  of  the  lower.  There  is  usually  mouth 
breathing  due  to  some  form  of  nasal  obstruction. 


Fig.  162 


Division  I. — The  characteristic  exists  on  one  side  only,  the  other 
being  normal.     Mouth  breathing  is  usually  associated  (Fig.  153). 

Division  II. — There  is  distal  occlusion  on  both  sides,  but  the  upper 
incisors  are  retruded  instead  of  protruded,  with  crowding  in  the  cuspid 
region.     These  are  associated  with  normal  breathing  (Fig.  154). 

Subdivision,  Division  II. — The  characteristic  is  upon  one  side  only; 
normal  breathers. 

Class  III.  Division  I. — In  this  class  the  lower  first  molars  occlude 
mesially  to  the  upper  first  molars  on  both  sides,  and  the  lower  jaw 
progressively  protrudes  anteriorly  (Fig.  155). 


THE  SECOND  DENTITION 


213 


Subdivision,  Class  III. — The  mesial  occlusion  is  upon  one  side  only, 
the  other  being  normal,  the  arches  crossing  in  the  region  of  the  incisors. 

Angle  has  formulated  the  law  "that  the  best  balance,  the  best 
harmony,  the  best  proportions  of  the  mouth  in  its  relations  to  the  other 
features  require  that  there  shall  be  the  full  complement  of  teeth,  and 
that  each  tooth  shall  be  made  to  occupy  its  normal  occlusional 
relations. 

The  specific  causes  inducing  malocclusion  of  the  teeth  as  classified 
above  are: 

.      Fig.  153 


Malocclusion.      Class  II. 


1.  Premature  loss  of  deciduous  teeth  prevents  the  pressure  of  the 
first  molars  upon  the  teeth  anterior  to  them,  which  mechanically  aids 
in  the  development  of  the  jaws  and  thus  of  the  space  necessary  for 
accommodation  of  the  permanent  teeth.  It  also  allows  the  first 
molar  to  drift  forward  and  come  into  malocclusion,  and  also  to 
close  the  space  occupied  by  the  deciduous  tooth,  thus  lessening 
space  for  its  succe.s.sor  and  forcing  it  into  buccal  or  lingual  displace- 
ment. The  same  is  true  of  loss  of  approximal  tooth  contact  as  the 
result  of  caries. 


214 


DENTITION 


2.  Prolonged  retention  of  deciduous  teeth  may  cause  a  deflection 
of  the  temporary  successor  or  prevent  its  eruption. 

3.  Through  loss  of  permanent  teeth  on  that  side  upon  which  the 
tooth  is  extracted  the  development  of  the  jaw  will  be  prevented  and 
the  tooth  posterior  to  the  space  will  tend  to  tip  or  drift  forward  into 
malocclusion. 

Fig.  154 


Malocc.usion.      Class  II.      Division  II. 


4.  Tardy  eruption  of  permanent  teeth  permits  closure  of  the  space 
altogether  or  in  part,  and  the  resistance  offered  causes  a  deflection  of 
the  tardy  tooth.  The  total  absence  of  certain  permanent  teeth  may 
be  placed  under  this  heading  (Fig.  156). 

5.  Supernumerary  teeth,  by  occupying  space,  also  compel  the 
normal  teeth  to  take  an  abnormal  position,  and,  if  erupting  after 
them,  may  displace  them  by  constant  pressure  (Figs.  191  and  216). 

6.  Habits  such  as  thumb  and  lip  sucking  or  lip  biting  will  move  the 


THE  SECOND  DENTITION  215 

upper  anterior  teeth  outward  and  the  lower  anterior  teeth  inward. 
Holdintr  the  tongue  between  the  anterior  teeth  prorhiees  infra-ocehision 
of  the  anterior  teeth,  while  the  constantly  open  mouth  permits  supra- 
occlusion  of  the  molars. 

7.  Nasal  obstructions  occurring  in  the  developing  child  produce 
mouth  breathing,  and  the  opening  of  the  mouth  causes  contraction 
of  the  muscles  upon  the  teeth  and  bones,  producing  abnormalities  of 
the  bone  of  the  jaw,  the  irregularity  of  Class  II  (Division  I),  an 
undeveloped  nose  and  adjacent  region  of  the  face. 

The  consideration  of  malocclusion  as  a  general  subject  is  properly 
relegated  to  special  works,  and  the  reader  is  referred  to  Angle's 
Malocclusion  of  the  Teeth  and  other  works  on  the  subject. 

Fig.  155 


Malocclusion.      Class  III. 

Disorders  of  the  Second  Dentition.— Tlie  devitalization  of  the 
pulp  of  a  temporary  tooth  antl  j)r()per  canal  filling  delays,  but  does  not 
absolutely  prevent,  resorption.  Chronic  abscesses  upon  such  roots 
destroy  the  resorbent  organ,  but  some  pathological  resorption  may 
occur,  as  in  case  of  permanent  roots  (which  see).  Pus  has  an  alkaline 
reaction  which  may  neutralize  tiie  acid  solvent.  As  a  rule,  such  roots 
are  mechanical  obstructions  to  the  permanent  crowns,  which  are 
deflected  to  one  side  and  caused  to  erupt  irregularly;  again,  the  tempo- 
rary root  may  be  bodily  pushed  asiile,  its  apex  pressed  against  the 
alveolar  process  and  gum  tissue,  which  are  resorl)ed,  and  the  necrotic 
root  end  is  seen  extruded  through  the  gum.     Extraction  is  indicated. 

When  temporary  roots  are  not  thus  mechanically  removed  they  are 
gradually  extruded  and  decayed,  or  suppurative  processes  cause  the 
resorption  of  the  alveolar  process  about  them. 


216  DENTITION 

Injudicious  retention  of  temporary  teeth  may  thus  cause  an  irregu- 
larity. On  the  other  hand,  premature  extraction  by  permitting  the 
approximation  of  the  previously  erupted  permanent  teeth  may  have 
an  equally  bad  effect  upon  an  erupting  tooth  (Fig.  156). 

In  anticipation  of  physiological  resorption  of  temporary  roots,  all 
temporary  teeth  should  be  carefully  watched,  cleansed,  filled,  and,  if 
necessary,  their  roots  treated  so  that  a  normal  replacement  by  the 
permanent  teeth  may  occur.  If  pronounced  disease  occur  just  pre- 
vious to  the  time  for  normal  replacement,  extraction  is  indicated. 

It  will  be  recalled  that  the  teeth  are  an  evolution  of  the  dermoid 
system,  which  fact  possesses  pathological  significance  in  certain  acute 
specific  skin  diseases.  It  is  noted  in  some  cases  of  the  eruptive 
fevers  of  children,  particularly  when  the  child  is  much  debilitated,  that 
after  the  cessation  of  the  acute  disease  a  necrotic  affection  of  the  jaw 

occurs,  involving  the  alveolar  bone  and  its 

Fig.  156  coutcnts.    As    many  of   these   cases    occur 

.-•^•:t/-v;v{ii^V'::.  between  the  ages  of  three  and  seven  years, 

•'•>.'.•. v.-:-:-,;,    il.".'.:-.'.  ^j^g  temporary  teeth  are  still  in  situ;  these, 

with  the  partially  developed  permanent  teeth 

and  the  enclosing  bone,  may  be  exfoliated. 

The  necrotic  process  may  involve  but  one 

tooth,  or  may  include  all  of  the  temporary 

teeth,  their  successors,  and  a  large  mass  of 

Effects  of  the  premature  loss  of      ,  ,       rm        t  -ji        i  •   i    xI  • 

a  deciduous  second  molar.  boUC.        The  dlSCaSC  With  whlch  thlS  UCCrOSlS 

is  most  frequently  associated  is  scarlet 
fever;^  it  is  also  found  as  a  sequel  of  measles  and  smallpox.  (See 
Chapter  IX.)  "The  cases  prior  to  exfoliation  of  the  bone  exhibit  a 
stripping  of  the  periosteum,  apparently  beginning  about  the  necks  of 
the  teeth.  A  discharge  of  pus  having  a  fetid  odor  is  present,  and  the 
soft  tissues  may  be  raised  from  the  bone  for  a  variable  extent;"  that  is, 
there  is  evidence  of  purulent  periostitis.  In  the  course  of  some  weeks, 
six  or  eight,  the  necrotic  bone  and  its  contents  exfoliate.  Salter 
observes  that  the  sequestra  forming  after  severe  scarlet  fever  are 
much  more  extensive  than  those  which  form  as  a  sequel  of  measles. 

The  administration  of  mercurials  has  been  credited  with  such  a 
loss  of  teeth  and  process.  I  have  seen  a  sequestrum  contain- 
ing three  teeth  attributed  to  this  cause.  In  these  cases  the  parts 
should  be  kept  as  aseptic  as  possible  by  means  of  hydrogen  dioxide 
and  the  compound  tincture  of  capsicum  and  myrrh  (enough  to  cloud 

1  Salter,  Dental  Pathology.  ^  ibid. 


THE  SECOND  DENTITION  217 

a  glass  of  water)  used  as  a  stimulant  mouth  wash.^  AVhen  loose,  the 
sequestrum  should  be  removed.  The  parts  heal  by  granulation  if 
due  attention  be  paid  to  the  general  physical  welfare  of  the  child. 

Eruption  of  the  Molars.— The  first  permanent  molars  rarely 
produce  more  tlian  slight  rheumatic  pains.  The  gum  irritation  may 
be  relieved  by  an  X  incision,  or  at  times  by  the  application  of 
phenolsodique  and  laudanum,  equal  parts,  with  the  finger-tip.  A 
little  alcohol  or  dilute  tincture  of  iodine  serves  almost  equally  well. 

As  some  time  may  elapse  between  eruption  and  occlusion,  the  first 
molars  do  not  receive  a  proper  friction.  Associated  frequently  with 
carious  temporary  teeth,  they  are  frequently  decayed  in  their  sulci  and 
fissures;  to  present  this  it  has  been  recommended  that  ox}'phosphate 
of  zinc  be  placed  over  these  fissures  without  previous  excavation.^ 

The  lower  second  molars  may  cause  some  irritation  owing  to  an 
insufficient  development  of  the  jaw  at  the  angle,  leaving  an  inadequate 
accommodation  for  the  crown.  At  about  nine  years  of  age  the  second 
molar  occupies  the  angle  of  the  jaw  in  much  the  same  position  as 
shown  in  Fig.  106  for  the  third  molar.  If  held  back  a  pathological 
condition  equivalent  to  that  occurring  in  the  temporary  teeth  may 
result;  reflexes  producing  heavy  pains  about  the  jaw  or  reflex  effects, 
such  as  chorea,  may  be  produced. 

Truman^  has  prevented  a  threatened  second  attack  of  this  sort  by 
deep  incisions  in  the  gum  over  the  site  of  the  crown.  The  presump- 
tion is  that  such  treatment  relieves  the  tension  upon  the  pulp  under- 
lying the  developing  root. 

Kirk*  calls  attention  to  the  liability  of  chorea  to  be  associated  with 
reflexes  from  the  dental  region  at  from  four  to  nine  years  of  age,  and 
cites  a  case  from  the  practice  of  C  N.  Peirce  in  which  choreic  mani- 
festations were  permanently  relieved  by  the  removal  of  a  deciduous 
molar  interfering  with  the  eruption  of  its  permanent  successor,  the 
bicuspid.  He  also  cites  a  case  of  repeated  hysterical  manifestations 
following  nervous  irritability  due  to  each  replacement  of  a  deciduous 
tooth  by  its  successor.  Flagg  cured  a  case  of  chorea  in  a  boy,  by 
the  extraction  of  four  teeth  from  a  very  crowded  arch.^ 

The  third  molars  frequently  induce  pathological  conditions. 

The  upper  third  molar,  meeting  in  its  descent  the  roots  of  the  second 
molar,  may  be  united  to  it  by  hypercementosis — the  condition  of  con- 
crescence  (which  see);  escaping  this,  it  may  meet  a  dense  palato- 

^  Garretson,  A  System  of  Oral  Surgery.  *  L.  Ashley  Faught. 

'  International  Dental  Journal.  1899.  *  Dental  Cosmos,  1905. 

'  Private  Communication. 


218  DENTITION 

alveolar  plate  of  bone  at  the  tuberosity  and  be  deflected  buccally 
through  the  thinner  buccal  plate  of  bone,  so  that  its  occlusal  face 
presents  cheekward  (Fig.  157).  Its  occlusal  face  may  present  more 
posteriorly  or  more  anteriorly.  Here  retained  food  collects  about 
it  and  caries  occurs,  or  a  suppurative  inflammation  of  the  cheek 
or  free  gum  margin  may  occur.  For  this  condition  sterilization,  free 
incision  of  the  gum  margin,  and  subsequent  asepsis  maintained  by 
antiseptic  sprays  will  reduce  the  inflammation,  which,  however,  is 
apt  to  recur  at  intervals.  If  the  cheek  be  irritated  or  the  position  of 
the  tooth  permanently  fixed,  only  traction  of  the  tooth  into  a  correct 
position,  grinding  away  of  the  sharp  cusps,  or  extraction  will  alleviate 
the  condition.  The  extraction  of  such  a  tooth  is  little  loss  to  the 
individual.  The  possibility  of  concrescence  in  such  a  case  as  shown 
in  Fig.  157  must  be  considered  when  extraction  is  intended.  In- 
dividual motion  is  diagnostic  of  separate  teeth,  and  is  readily  induced 
by  pressing  a  strong,  thin,  flat-bladed  instrument  between  the  teeth. 

Fig.    157  Fig.  158 


Abnormal  eruption  of  the  upper  third  Partial  eruption  and  impaction  of  third 

molar.  molar.      (Skiagraph  by  Custer.) 

The  pressure  of  an  erupting  third  molar  upon  the  second  molar 
may  cause  neuralgic  pains,  and  at  times  the  teeth  in  general,  as  far 
forward  as  the  central  incisor,  may  seem  to  loosen  up  and  become 
tender  to  touch  and  again  become  comfortable  and  tight.  These 
symptoms  may  be  repeated  apparently  in  consonance  with  the  efforts 
at  eruption. 

Owing  to  insufficient  development  at  the  angle  of  the  jaw,  it  is 
almost  the  rule  that  the  eruption  of  the  lower  third  molar  is  attended 
with  some  degree  of  discomfort  due  to  gum  and  bone  irritation,  and, 
possibly,  to  pressure  on  the  formative  pulp  (Fig.  106) . 

For  some  months  prior  to  eruption  heavy,  gnawing,  rheumatic  pains 
may  be  indefinitely  located  about  the  jaw  and  ear  of  the  affected  side. 
The  muscles  of  mastication  become  stiff  and  may  contract  spasmodic- 
ally, simulating  trismus.  These  symptoms,  if  severe,  may  be  relieved 
by  deep  X  incisions  in  the  gum;  or,  if  mild,  by  the  application  of  non- 


THE  SECOND  DENTITION  219 

discoloring  rubefacients  or  sedatives  to  the  outside  of  the  face,  over 
the  affected  parts.  The  massage  of  the  parts  affords  some  reUef. 
Flagg  recommended  the  following: 

IJ. — Tinct.  opii, 

Tinct.  aconiti, 

Chloroform! aa         q.  s.  — M. 

Sig. — To  be  rubbed  on  the  out. side  of  the  faee. 

Or, 

I^. — Aconitine gr.  j 

Cerat.  simp 5J — M. 

Sig. — To  be  well  spatulated.     To  be  distended  with  oil    of    cloves    or    eamiihnphenique 
and  gently  rubbed  on  the  outside  of  the  face,  the  mouth  and  eyes  to  be  particularly  avoided. 

Or,  when  the  aconitine  fails  to  produce  relief: 

I^  — Veratrine gr.  xx 

Cerat.  simp 3i — M. 

Sig. — To  be  used  in  the  same  manner  as  the  aconitine. 

As  the  tooth  advances  the  symptoms  may  become  progressively 
severe.  The  gum  may  become  inflamed,  swollen,  and  be  masticated 
upon,  the  oral  pyogenic  organisms  produce  infection,  presumably  find- 
ing an  entrance  at  the  point  proximating  the  second  molar.  The 
patient  suffers  from  the  pain  and  inability  to  masticate,  and  becomes 
nervous,  irritable,  and  debilitated;  the  breath  becomes  fetid  and  the 
salivation  excessive.  The  inflammation  extends  into  the  contigiunis 
tissues,  and  pus  may  form  extending  into  them;  all  mastication  is 
prevented,  fever  is  present,  and  the  patient  prostrated;  septicemia 
and  death  may  follow.^ 

Results  similar  to  these  may  occur  wIumi  the  crown  is  partly  erupted, 
being  covered  at  its  distal  portion  by  a  curtain  of  gum  which  may  be 
ulcerated  upon  its  under  surface.  This  curtain  of  gum  may  be  thin 
and  stretched  or  project  rather  rigidly  over  the  tooth  without  stretching, 
as  though  attached  to  it. 

In  these  latter  cases  the  pus,  as  a  rule,  finds  egress,  but  occasionally 
it  burrows  into  the  pocket  between  the  tooth  and  contiguous  tis.sue, 
causing  much  inflammation. 

Treatment. — The  treatment  depends  u]U)u  the  stage  to  which  the 
inflammation  has  advanced. 

If  the  patient  be  able  to  partly  open  tiie  moutli,  the  part  may  be 
sterilized  by  spraying  it  with  a  germicide  such  as  a  1  to2t)00  solution 
of  mercuric  chloride  in  hydrogen  dioxide.  Following  this  an  injection 
of  cocaine  solution  is  made  into  the  flap  of  tissue  and  the  gum  com- 
pletely removed  from  over  the  face  of  the  crown,  or,  if  feasiiile,  aiiy 
pocket  wall  cut  away. 

'  Flagg,  and  occasioual  reijorts. 


220  DENTITION 

To  accomplish  this  a  deep  linear  cut  is  made  with  a  sharp  bistoury 
extending  from  the  distolingual  to  the  mesolingual  angle  of  the  crown 
A  similar  cut  is  made  from  the  distobuccal  to  the  mesobuccal  angle. 
If  not  already  free,  the  gum  is  divided  at  its  mesial  contact  with  the 
distal  surface  of  the  second  molar.  The  block  is  now  penetrated  by 
a  tenaculum,  drawn  tense,  and  the  final  cut  made  at  the  distal  border 
with  decidedly  curved  gum  scissors.  Less  cutting  is  required  in 
some  cases. 

The  hydrogen  dioxide  spray  should  be  again  applied  to  remove  any 
possible  pus  germs  present,  and  should  be  repeated  at  intervals  of 
about  two  hours.  A  neglect  of  this  simple  precaution  gave  the  editor 
a  week  of  personal  discomfort  and  inability  to  masticate  after  the 
removal  of  a  trifling  and  apparently  non-inflamed  flap  of  gum.  A  cold 
compress  should  be  recommended  for  the  angle  of  the  jaw  if  deemed 
advisable.  Magnesium  sulphate  as  a  derivative  may  be  used  with 
advantage. 

If  the  patient  be  confined  to  his  bed  and  unable  to  open  the  jaws, 
a  more  difficult  operation  presents.  The  first  object  should  be  to 
reduce  the  intensity  of  the  inflammatory  symptoms.  This  is  accom- 
plished by  the  removal  of  the  gum  block  as  above,  if  the  mouth  can 
be  opened  sufficiently.  Etherization  may  be  resorted  to,  after  oral 
sterilization,  for  the  purpose.  A  jaw  separator  is  introduced  and 
operated  until  sufficient  space  is  gained  and  the  cuts  made.  If  no 
more  be  possible  at  the  first  visit,  the  lingual  and  buccal  linear  cuts 
should  be  made  to  insure  free  bloodletting,  which  may  be  increased 
by  syringing  forcibly  with  lukewarm  water,  the  position  of  the  patient 
being  such  that  gravity  favors  its  flowing  out  of  the  mouth. 

Cold  compresses  are  to  be  placed  over  the  angle  of  the  jaw  and 
magnesium  sulphate  and  the  hot  pediluvium  administered  as  deriva- 
tives. Cataplasma  kaolini,  a  compound  of  kaolin  (Chinese  clay) ,  boric 
acid,  methyl  salicylate,  glycerin,  and  small  quantities  of  thymol  and 
oil  of  peppermint,  is  useful  applied  in  quantity  to  the  face  externally. 
The  antiseptic   sprays  are  to  be  used  as  before  directed. 

If,  in  addition,  local  massage  over  the  angle  of  the  jaw  be  practised, 
the  swelling  and  muscular  hardness  usually  disappear  in  a  few  days.  It 
is  well  to  then  remove  the  entire  block  of  gum  to  prevent  re-infection. 

If  the  third  molar  be  correctly  placed,  its  eruption,  as  a  rule,  proceeds 
uninterruptedly  from  this  point,  though  it  may  never  be  entirely  free 
from  some  degree  of  overlapping  by  the  gum  tissue,  owing  to  arrest 
of  eruption  by  the  occlusion  of  the  more  advanced  upper  third  molar. 


THE  SECOND  DENTITION  221 

Pockets  are  thus  formed  which  favor  food  retention,  which,  undergoing 
fermentation,  may  either  cause  ulceration  of  the  soft  parts  or  caries  of 
the  distal  and  distobuccal  surfaces  of  the  tooth. 

More  marked  malposition  may  cause  difficulty  of  eruption,  necessi- 
tating the  extraction  of  the  third  molar  or  even  of  the  second  molar. 

In  some  cases  it  may  be  better  to  also  extract  the  upper  third  molar, 
as  it  will  probably  elongate  in  time  and  allow  food  to  pack  into  the 
interspace  mesial  to  it. 

A  presentation  of  the  occlusal  face  of  the  third  molar  to  the  distal 
surface  of  the  second  molar  is  a  common  form  of  malposition. 

If  very  deep  seated  the  third  molar  may  at  times  be  diagnosticated 
in  this  position  by  passing  an  explorer  or  thin  right-angled  blade  down 
the  distal  surface  of  the  second  molar,  or  by  means  of  a  deep  incision 
with  a  bistoury  or  exploring  needle.  Failing  this,  or,  preferably, 
replacing  it,  the  x-rays  are  a  very  valuable  means  of  diagnosis. 

In  this  situation  pathological  resorption  of  the  root  of  the  second 
molar  may  residt,  and  irritation  of  its  pulp  be  added  as  a  com- 
plication. In  this  case  the  second  molar  must  be  extracted.  (See 
Malposition.) 

A  more  common  form  of  presentation  exhibits  the  distal  surface  of 
the  crown  above  the  gum  and  the  mesoocclusal  angle  locked  beneath 
the  cervix  of  the  second  molar  (Fig.  158).  The  third  molar  may  be 
removed  by  an  operation  involving  the  surgical  removal  of  a  portion 
of  the  base  of  the  coronoid  process  followed  by  extraction.  The  pulp 
of  the  third  molar  may  be  devitalized  by  arsenic  applied  and  sealed  in 
a  pit  drilled  in  its  distal  surface.  After  death  of  a  portion  of  the  pulp 
the  pit  may  be  made  to  perforate  the  crown  from  side  to  side,  and 
then  a  dentate  fissure  bur  mounted  in  the  right-angle  handpiece  or  a 
disk  may  be  used  to  saw  off  the  occlusal  half  of  the  crown.  In  the 
space  thus  gained  and  between  the  second  and  third  molars  a  wedge 
of  sea-tangle  may  be  neatly  fitted;  its  swelling  causes  mutual  sepa- 
ration, which  loosens  the  third  molar  somewhat  by  the  process  of 
resorption.  It  should  now  be  quite  readily  extracted  by  appropriate 
movements. 

Cryer  recommends  the  removal  of  the  occlusal  section  of  the  crown 
of  the  third  molar  by  means  of  a  carborundum  disk,  and  the  removal 
of  the  tooth  by  means  of  forceps  or  elevators. 

The  loss  of  a  second  molar  may  be  for  other  reasons  necessary, 
but  such  a  loss  in  the  last  case  described  is  equivalent  to  a  loss  of 
two  teeth,  as  the  third  molar  will  be  of  little  value. 


CHAPTER    VIII. 
MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Abnormalities  of  the  teeth  are  found  associated  with  position^,  size, 
form,  and  structure.  Aberrations  in  form,  structure,  and  size  are 
inckided  under  the  head  of  malformations  of  the  teeth;  aberrat  ons  of 
position  are  discussed  under  the  head  of  malpositions  of  the  teeth. 
The  particular  section  of  dentistry  relating  to  malpositions  of  the 
teeth  is  by  general  consent  made  a  special  department  of  operative 
dentistry,  that  of  orthodontia;  but  many  of  the  phases  of  the  subject 
are  of  great  pathological  interest,  although  the  therapeutic  measures 
usually  demanded  are  mechanical  in  character  and  clearly  belong  to 
the  fields  of  operative  and  prosthetic  dentistry. 

Malformations  of  the  teeth  may  be  macroscopic  or  visible  to  the 
naked  eye,  or  microscopic,  requiring  special  preparation  for  observa- 
tion under  the  microscope. 

The  causes  of  imperfectly  formed  enamel  or  teeth  must  be  sought 
by  study  of  the  conditions  preceding  their  development.  That  modi- 
fications of  general  nutrition  must  modify  tooth  development  seems 
to  be  a  safe  proposition. 

An  ill-nourished  child  is  apt  to  have  at  least  poorly  organized  tooth 
material,  while  in  one  that  has  actually  undergone  an  exanthematous 
disease  the  tooth  form  subsequently  seen  seems  frequently  to  have 
been  profoundly  modified  by  the  disease. 

MICROSCOPIC    MALFORMATIONS, 

Microscopic  or  histological  defects  of  the  teeth  may  affect  any  of  the 
dental  tissues,  enamel,  dentine,  cementum,  pulp,  or  pericementum. 

Enamel. — Defects  in  enamel  structure  range  from  any  degree  of 
orderliness  in  the  even  distribution  of  globular  bodies  and  cementing 
substance  in  the  tissue  to  gross  aberrations  in  formation.  The  finer 
variations  of  structure  are  not  easily  recognizable. 

Theoretically  perfect  enamel  should  show  in  longitudinal  section  a 
series  of  squares  of  uniform  size  built  into  rods,  the  spaces  between  the 


MICROSCOPIC  MALFORMATIONS 


223 


squares  and  rods  being  marked  by  lines  of  cementing  substance  having 
a  refractive  index  slightly  different  from  that  of  the  squares  (Fig.  113). 
While  such  a  structure  is  perhaps  never  found,  it  is  difficult  to  draw  a 
line  where  aberrations  from  such  a  standard  become  pathological. 
An  arbitrary  standard  might  be  assumed  as  follows:  Regard  any 
enamel  as  pathological  where  areas  of  it  differ  from  its  general  sub- 
stance to  such  an  extent  as  to  have  a  decidedly  different  refractive 


Fig.  159 


W  if'  *«  ■  ''^l^'^         * 

^ 

•'%f«ii' 

«». 

*  * 

A 

^                                        :?.^^^ 
*        '          ^          .^1*            ♦ 

'? 

-*^', 

V 

•*... 

^       ^ 

-*^ 

'      'k   #f  - 

^«*%-A;; 

^     *'    •' 

■♦  . 

/ 

Portion  of  a  white  spot  in  enamel,  showing  lack  of  interprismatic  cement  substance. 
X  2000.     (Williams.) 


index.  A  typical  form  of  abnorma  ity  is  noted  in  what  are  known  as 
white  spots  of  the  enamel,  areas  in  which  an  opaque  surface  exists 
instead  of  the  normally  translucent  enamel. 

Opaque  Spots  in  Enamel. — White,  brown,  and  corn-colored  opaque 
areas  of  enamel  are  frequently  seen  surroundeil  by  apparently  normal 
enamel. 

Examined  without  the  aid  of  the  microscope  they  are  seen  to  present 
a  surface  as  smooth  as  any  enamel,  but  upon  tliis  surface  being  broken 


224     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

up  with  a  bur  a  chalky,  granular,  whitish  material  containing  at  times 
the  yellowish  pigment  is  seen  sometimes  occupying  the  entire  thickness 
of  the  enamel.  These  spots,  if  slight,  are  sometimes  without  this 
granular  character,  while  the  pigment  affects  the  entire  thickness  of 
the  enamel. 

Williams  submitted  the  enamel  at  the  bo  ders  of  such  spots  to 
microscopic  examination,  and  compared  it  with  enamel  in  the  first 
stages  of  decay,  finding  in  both  a  similar  appearance  characteristic 
of  a  lack  of  or  a  loss  of  interprismatic  cement  substance  (Fig.  159). 

Fig.  160 


Section  through  human  cuspid,  showing  sulcus  and  appearance  of  tissue  in  its  vicinity. 
X  75.     (Specimen  by  Choquet;  photo,  by  Williams.) 


Upon  the  data  derived  from  his  investigations  with  the  development 
of  the  enamel  he  concluded  that  these  spots  are  due  to  a  lack  of  such 
cement  substance.  This  leaves,  as  the  probable  substance  in  the  spot, 
unfused  globules  mingled  with  some  pigment.    • 

Enamel  formation  about  the  sulci  of  teeth  is  frequently  faulty; 
owing  to  an  imperfect  union  of  the  enamel  segments  forming  the  cusps 
of  the  teeth,  minute  fissures  exist  in  the  enamel;  these  are  most  marked 
in  the  fissures  of  molars,  as  shown  in  Fig.  160.  The  enamel  bounding 
these  fissures  has  an  irregular  structure. 


MICROSCOPIC  MALFORMATIONS 


225 


The  dentinal  fibrillae  may  penetrate  the  substance  of  the  enamel 
(Fig.  161),  occupying  defined  channels  in  its  substance;  this  is  re- 
garded by  Williams  as  a  developmental  accident.  He  pointed  out  that 
the  organic  filaments  from  the  dentine  become  atrophied  with  the 
progress  of  enamel  formation  and  canals  remain.  Caush*  claims 
to  have  found  this  to  be  a  normal  condition  of  human  enamel,  and 

Fig.  161 


■•  '".■ 


■*^' 


!&J  .('■  ■  ■" 


f    *•» 


^i% 


\       > 


A(  AV  ',  \ 


Section  of  human  molar,  showing  dentinal  fibrilUe  penetrating  enamel.     X  COO.     (.Williams.) 

regards  these  as  nutrient  spaces.  They  may  form  cloud-like  mark- 
ings (stripes  of  Schreger  in  enamel,  Fig.  1G4).  This  condition,  as 
also  many  other  variations  of  structure  found  in  the  dental  tissues  of 
man,  are  shown  by  Williams  to  have  their  normal  prototypes  in  the 
dental  tissues   of  lower  animals;  for  example,   the  penetration    of 


'  International  Dental  Journal,  June,  1904. 


15 


226     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

dentinal  fibrillse  into  enamel  is  a  normal  condition  in  the  teeth  of 
the  kangaroo.  Such  conditions  are  not  to  be  confounded  with 
fissures  of  enamel  where  large  lines  of  faulty  calcification  or  non- 
calcification  extend  through  the  thickness  of  enamel.  A  portion  of 
the  enamel  may  occupy  an  area  within  dentine. 

Enamel,  even  normal  enamel,  is  not  of  uniform  composition;  were 
it  so,  it  would  exhibit,  in  addition  to  an  orderly  arrangement  of  its 
histological  elements,  a  uniformity  in  color.  So  common  are  diflFer- 
ences  in  this  direction  that  the  presence  of  pigment  bands  must  be 

Fig.  162 


Section  of  human  incisor,  showing  "bands  of  Retzius"  and  marked  stratification  of 
enamel.      X  125.     (Williams.) 

regarded  as  normal.  It  is  the  rule  to  find  enamel  traversed  by  deeply 
pigmented  parallel  bands,  which  pass  obliquely  upward  from  the 
surface  of  the  dentine  to  the  surface  of  the  enamel.  These  are  termed 
the  bands  of  Retzius;  they  appear  to  mark  the  size  of  the  enamel 
cap  at  successive  periods  of  its  growth  (Fig.  162). 

Stratification  and  striation  of  the  enamel,  as  shown  by  Williams, 
must  be  regarded  as  normal  physiological  records  of  the  mode  of 
enamel  formation.  Kirk  has  shown  that  normal  enamel  shows  vari- 
ations in  density  in  the  same  teeth. 


MICROSCOPIC  MALFORMATIONS 


227 


All  of  these  histological  defects  represent  variations  of  deposition, 
no  doubt  due  to  fluctuations  of  the  nutritive  processes  of  the  child  at 
the  time  of  tooth  formation.  Histological  records  made  in  the  enamel 
are  not  like  those  made  in  other  tissues,  for  there  is  no  certain  provision 
tlirough  which  such  defects  can  be  remedied  at  subsequent  periods- 
Profound  nutritive  disturbances,  such  as  those  attending  hereditary 
syphilis  in  children,  affect  the  structures  of  the  teeth.  One  of  the  gross 
results  of  this  disease  is  a  common  malformation  of  the  general  form  of 
(he  incisors.     The  hard  tissues  of  such  teeth  exhil)it  microscopic  evi- 


FiG.  163 


Section  of  enamel  from  syphilitic  tooth,  with  appearances  resembling  the  laoima;  of 
cementum.      X  GOO.     (Williams.) 

dences  of  faulty  histology;  they  are  dull  and  opaque  and  traversed  by 
irregular  bands.  Viewed  in  section,  the  enamel  of  such  teeth  is  seen  to 
be  almost  structureless  (Fig.  163).  Williams  found  that  the  contents 
of  the  large,  irregular  spaces  in  this  enamel  did  not  respond  to  stains — 
i.  e.,  did  not  contain  organic  matter. 

There  is  evidence  that  other  forms  of  specific  dermatitis — scarlet 
fever  and  measles — which  occur  at  an  early  age  may  affect  the  for- 
mation of  enamel.  The  defects  attributed  to  the  exanthemata  are 
irregular  pits  upon  the  crowns  of,  particularly,  the  incisors  (Fig.  174), 
though  the  cuspids  and  first  molars  also  suffer.  In  some  cases  the 
crowns  appear  honey-combed.  The  condition  is  known  as  hypoplasia 
of  the  enamel,  and  is  evidently  due  to  an  effect  upon  the  enamel  organs. 


228     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

There  is  evidence  in  some  specimens  (Fig.  171)  that  the  dentine  may 
be  hypoplastic,  the  papilla  being  doubtless  affected  by  the  prevailing 
systemic  malnutrition.  The  dentine  should  be  first  developed,  and 
without  doubt  is  so  developed  in  simple  cases  of  hypoplasia,  therefore 
the  dentine  may  be  normal  in  form,  except  for  microscopically  evident 
disturbance,  as  in  the  formation  of  interglobular  spaces,  while  the 
enamel  is  hypoplastic  (Fig.  171). 

As  cases  occur  in  which  distinct  columns  of  enamel  may  be  formed 
in  dentine,  the  record  is  one  of  a  heterogeneous  mixture  of  the  two 

Fig.  164 


^--^ 

"^ 

/       ^ 

•»  \f,' 

?w 

f  ^  ^ 

m 

^k 

"T^^'  '"f^jjk 

wi 

W--^^% 

i 

W 

~^^^s^^^ 

^^^^m 

m 

^ 

w 

Enamel  and  dentine,  human  tooth:  1,  enamel;  2,  dentine;  3,  lines  of  Schreger  in  enamel; 
4,  brown  strise  of  Retzius.  (Probably  aggregation  of  tubes,  editor.)  (Broomell,  after 
Geise.) 


formative  tissues  (enamel  organ  and  papilla),  while  in  the  plastic  state 
the  condition  is  evidenced  by  such  an  abnormality  as  an  odontoma. 

Black  regards  the  formation  of  pits,  the  simultaneously  developed 
zone  of  enamel  being  perfect,  as  due  to  aberration  in  development  of 
enamel  rods,  leaving  a  hole  (doubtless  a  localized  effect  upon  the 
ameloVjlasts) .  Histologically  the  strata  of  the  enamel  partly  fail  of 
deposition  at  these  points  (Fig.  171). 

With  a  history  of  a  case,  including  the  age  of  the  child  at  the  period 
of  the  disease,  if  examination  be  made  of  the  positions  of  the  defects, 
the  age  will  serve  as  an  indication  as  to  whether  there  has  been  any 


MICROSCOPIC  MALFORMATIONS  229 

connection  between  the  eruptive  fever  and  the  dental  malformation. 
For  example,  if  enamel  pits  upon  incisors  have  been  caused  by  an 
eruptive  fever  between  the  ages  of  four  or  five,  they  should  occupy 
a  part  a  little  above  the  half-way  area  of  the  crown  face  or  a  central 
incisor;  it  is  evident  that,  the  enamel  being  already  formed  about  the 
cutting  edge  of  the  tooth,  alterations  of  nutrition  could  not  affect  the 
already  formed  tissue;  the  later-formed  enamel  may  be  perfect  (Fig. 
173).  In  cases  where  a  causal  association  of  enamel  defects  with  the 
eruptive  fever  is  made  out  with  reasonable  clearness,  it  is  usual  to 
find  all  of  the  crowns  of  the  teeth,  which  are  in  process  of  formation, 
affected  in  a  similar  manner,  but  at  different  levels,  according  to 
progress  of  enamel  development. 

Fig.  165 


C^''"-VrV'r  -r  '^    \V. 


e 

Section  of  a  bicuspid  with  its  alveolus,  showing  a  pit-like  absorption  upon  the  side  of  the 
root  in  which  the  redeposit  of  the  cementum  has  begun:  a,  dentine;  6,  cementum;  c,  peri- 
dental membrane;  d,  bone  forming  the  wall  of  the  alveolus;  e,  absorbed  area  of  cementum. 
It  will  be  noticed  that  a  new  deposit  of  cementum  has  begun  the  filling  of  the  area,  and  that 
the  soft  tissue  in  the  area  of  absorption  is  of  a  cellular  type.  The  bone  also  shows  the  effects 
of  absorption  in  the  cutting  away  of  portions  of  the  rings  of  the  Haversian  systems  at  /,  while 
at  g  the  presence  of  osteoclasts  shows  that  absorption  is  in  progress  at  that  point.     (Black.) 

Cases  are  observed  where  there  has  been  a  formative  crisis  to  the 
extent  of  having  apparently  no  enamel  whatever  formed  over  the 
occlusal  section  of  the  crown,  its  deposit  on  the  remainder  of  tiie  crown 
being  quite  normal  (Fig.  173). 

D.  B.  Freeman^  records  the  case  of  an  individual,  aged  twenty-six 
years,  whose  teeth  anterior  to  the  second  molar  were  entirely  devoid 
of  enamel.  The  condition  was  hereditary;  it  appeared  in  both  brothers 
and  sisters,  and  could  be  traced  back  for  three  generations. 

Hopewell-Smitlr  claims  that  teeth  apparently  devoid  of  enamel 

1  See  Guilford,  American  System  of  Dentistry,  vol.  iii. 
'  Histology  and  Pathol.  Histology  of  the  Teeth. 


230     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

have,  in  all  cases  examined  by  him,  had  attenuated  enamel  upon 
them.     This  would  also  be  classified  as  hypoplasia. 

Black^  has  described  the  teeth  of  a  man,  aged  twenty-seven  years, 
as  having  enamel  of  an  opaque,  paper-white  appearance,  as  readily 

cut  as  a  slate  pencil,  and  with  den- 
Fi«-  ^66  tine  of  ordinary  consistence.     The 

"-"zf^--  >-—  ,-r--  \J^^^*f^  af»  teeth  presented   little  caries.     He 

^jT"^  ^  O"^^^  -  ?  Jb»i!^Xi.  also  described  the  temporary  teeth 

of  a  child  as  all  without  trace  of 
enamel,  the  dentine  soft,  bendable 
in  any  direction,  with  production 
of  pain,  and  penetrable  with  a  sharp 
explorer  (agenesia  of  enamel). 
Hopewell-Smith^  describes  the 
enamel  developed  during  rickets  as  faulty,  and,  in  so  far  as  limited 
observation  could  determine,  contained  numerous  spaces  probably 
filled  with  soft  tissue.  These  spaces  were  in  the  first-formed  portions 
of  the  specimens  observed. 

Fig.  167 


Dentinal  tubuli  terminating  in  the  spaces  of 
the  granular  layer.     (Tomes.) 


Section  showing  interglobular  spaces  in  dentine  of  a  syphilitic  human  tooth.     (Williams.) 

Dentine. — Data  regarding  the  finer  phases  of  defective  histological 
structure  of  the  dentine  are  meagre.     It  has  been  observed  that  the 


'  Dental  Cosmos,  June,  1898. 


2  Loo.  cit. 


MICROSCOPIC  MALFORMATIONS  231 

dentinal  tubuli  of  some  teeth  are  much  larger  than  in  others  of  the 
same  age,  and,  no  doubt,  future  investigations  with  an  improved 
technique  directed  toward  a  study  of  the  exact  mode  of  dentine 
formation  will  exhibit  defects  more  certainly. 

The  chief  histological  defects  noted  in  dentine  are  areas  of  faulty 
or  non-calcification,  called  interglobular  spaces.  (See  Chapter  VI.) 
These  are  most  common  in  the  dentine  immediately  underlying  its 
covering  tissue,  so  common  in  the  dentine  under  the  cementum  that 
this  portion  of  dentine  has  been  called  the  stratum  granulosum,  the 
granular  layer  of  Tomes  (Fig.  162).  In  the  body  of  the  dentine  these 
spaces  have  a  more  irregular  distribution. 

In  wet-ground  sections  (Rose)  the  dentinal  filaments  are  seen  to 
pursue  an  unbroken  course  through  these  areas.  The  contents  of  the 
interglobular  spaces  react  to  stains  like  the  sheaths  of  Neumann;  that 
is,  they  probably  contain  transitional  tissue.  These  areas  probai)ly 
represent,  as  do  defective  spots  of  enamel,  periods  of  depressed  vitality, 
or  of  altered  nutrition.  In  the  light  of  present  knowledge  regarding 
the  subject  they  are  to  be  viewed  as  areas  in  which  the  calcific  process 
was  faulty.  The  malformations  noted  in  connection  with  the  enamel 
of  teeth  have  their  analogues  in  the  dentine  (Fig.  167;  also  171). 

Interglobular  spaces  afford  some  evidence  of  the  formation  of 
dentine  by  a  deposition  of  globular  bodies  in  a  matrix  of  protoplasmic 
material.  Tiie  continuation  of  the  tubules  through  the  mass  of 
uncalcified  contents  is  evidence  of  their  independent  formation  by  the 
fibril  cells. 

Histological  malformations  of  the  pulp  have  not  l)een  recorded,  the 
normal  histology  of  the  organ  not  being  made  out  with  sufficient  cer- 
tainty to  determine  what  appearances  are  to  be  regarded  as  al)normal. 
Grosser  aberrations,  such  as  those  shown  in  P'ig.  131,  are  made  out. 

Cementum. — As  stated  in  Chapter  VI,  the  pericementum  contains 
numbers  of  multinucleated  cells — odontoclasts;  and  their  j)resence  is 
not  to  be  regarded  as  abnormal.  The  cementum  of  the  roots  of  teeth 
may  exhibit  evidences  of  former  action  of  these  cells  in  excavations  of 
cementum,  which,  by  a  subsequent  deposition  of  cementum,  have 
become  filled.  This  gives  an  irregular  course  to  the  cement  lamina? 
(Fig.  165).  These  appearances  are  to  be  regarded  as  not  necessarily 
pathological,  for  the  following  reason :  for  some  time  (years)  subse- 
quent to  the  eruption  of  the  teeth  developmental  changes  occur  in 
the  alveolar  bones;  depositions  (subperiosteal)  increasing  their  volume 
are  accompanied  by  resorption  of  other  portions  of  the  bone,  such  a 


232     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

balance  being  kept  between  their  processes  that  the  teeth,  although 
shifting  their  positions,  are  kept  in  normal  occlusion. 

The  cementum  may  be  thickened  by  additional  deposits,  as  in 
hypercementosis,  which  is  an  excess  of  development  classed  as  patho- 
logical. 

A  small  excrescence  may  be  found  upon  the  cementum,  and  is 
known  as  a  cemental  nodule. 


MACROSCOPIC   MALFORMATIONS. 

The  teeth  may  vary  from  the  normal  either  as  regards  size  or  external 
configuration. 

Variations  as  to  Size. — It  is  patent  to  the  most  casual  observer 
that  the  teeth  vary  as  to  size.  Comparisons  in  this  direction  are  made 
by  an  examination  of  the  upper  central  incisors.  Fig.  168  shows 
nearly  the  extremes  of  observable  sizes;  Guilford^  points  out  that 

Fig.  168  Fig.  169 


excessively  large,  central  incisor  crowns  are  usually  supported  by 
abnormally  small  conical  roots.  Marked  giantism  of  the  central 
incisors  usually  occurs  in  pairs,  the  other  teeth  being  of  normal  size. 
On  the  other  hand,  dental  giantism  of  less  degree  may  involve  all  of 
the  teeth  of  a  denture.  The  molar  teeth  are  occasionally  of  enormous 
size,  the  biscuspids  rarely  so,  and  the  cuspids  next  in  frequency  to 
the  molars  as  to  the  occurrence  of  giantism.  Guilford  observes  that 
giantism  of  the  cuspid  crowns,  unlike  that  of  the  central  incisors,  is 
usually  accompanied  by  an  increased  size  of  root.  He  mentions  the 
case  of  a  cuspid  measuring  an  inch  and  one-half  in  length  from  tip 
to  tip. 

Dwarf  Teeth. — Deficiency  in  size  is  of  more  common  occurrence 
than  excessive  size.  It  appears  to  occur  more  frequently  with  the 
upper  third  molars  and  upper  lateral  incisors  than  with  any  other 

•  American  System  of  Dentistry,  vol.  iii. 


MACROSCOPIC  MALFORMATIONS 


233 


teeth.     Fig.  169  shows  the  extremes  in  size  between  two  perfectly 
formed  lower  third  molars.     The  stunting  of  these  and  of  other  teeth 


Fig.  170 


Tusk-like  permanent  central  incisors;  temporary  teeth  retained  on  either  side. 
Lady,  aged  twenty-five  years. 


is,  however,  usually  associated  with  such  an  aberration  of  outward 
form  that  most  dwarf  teeth  must  be  considered  as  abnormal  in  form 

'  Fig.  171 


Hypoplasia  of  enamel,  showing  arrested  stratification;   dentine  shows  effects  of  hypoplasia  at 
interglobular  spaces.       (Hopewell-Smith.) 


as  well  as  in  size.     The  writer  has  seen  a  supernumerary  with  crown 
and  root  together  measuring  one-eighth  inch. 


234     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

Conical  Teeth. — ^The  primitive  tooth  is  composed  of  but  a  single  cone. 
Human  teeth  have  forms  which  are  modified  cones  or  combinations 
of  cones.  Return  to  a  conical  form  is  therefore  denominated  reversion 
to  a  primitive  type. 

A  central  incisor,  or  more  frequently  a  lateral  incisor,  may  have 
a  conical  crown,  as  shown  in  Fig.  170.     The  condition  may  be  double. 


Fig.  172 


Fig.  173 


Hypoplasia  due  to  eruptive  fevers.  Hypoplasia  of  incisal  portion  of  enamel. 

Upper  third  molars  frequently  consist  of  but  a  single  cone,  diminu- 
tive in  size;  at  times  a  crater-like  crown  is  formed  by  a  series  of  small 
cones  about  a  central  pit. 

Hypoplasia  of  the  Dental  Structures. — By  hypoplasia  in  this  con- 
nection is  meant  an  arrested  development  of  any  portion  of  a  tooth. 
Nutritional  disturbances,  the  exanthemata,  and  syphilis  all  seem  to 

Fig.  174 


Showing  the  front  teeth  grooved  from  tlie  alternation  of  perfectly  and  imperfectly 
developed  portions  of  enamel.     Hypoplasia.     (Tomes.) 


have  a  profound  influence  upon  the  form  of  teeth  developing  during 
the  period  of  active  disease.  With  the  passing  of  this  period  the 
development  of  the  tooth  may  proceed  in  an  orderly  manner. 

Pitted  and  Grooved  Teeth. — The  malformations  described  under 
this  heading  may  consist  of  a  series  of  irregular  grooves  or  pittings, 
the  crowns  having  approximately  the  normal  outlines. 

Of  these  malformations  Figs.  174  and  175  are  fairly  typical. 


MACROSCOPIC  MALFORMATIONS 


235 


Hutchinson's  Teeth. — During  the  first  few  weeks  after  birth  skin 
eruptions  characteristic  of  hereditary  syphiHs  are  apt  to  occur  in  the 
contaminated  chikl.     At  this  period  the  enamel  of  the  tips  of  the 


Fig.  175 


Malformations  of  incisal  half  of  crowns,  with  cervical  half  perfect.     Hypoplasia.     Attribu- 
table to  malnutritional  processes  rather  than  to  syphilis.     (Model  by  W.  A.  Capon.) 

permanent  incisors  is  undergoing  development  (see  Fig.  Ill)  and  the 
effect  of  the  eruption  is  to  cause  a  defective  development  at  this  point. 
Instead  of  the  normal  angles  and  flattened  curves  of  the  labial  surfaces 

FiQ.  176 


Pitted  and  fringed  teeth,  some  of  them  carious  at  the  incisal  edges.     Specimen  in 
museum  of  Philadelphia  Dental  College. 

the  incisors  may  have  a  roughly  rounded  and  stunted  appearance. 
The  incisal  edge  of  the  tooth  is  narrower  than  its  neck.  The  enamel 
at  this  edge  is  irregukirly  and  badly  formetl;  but  there  is  a  semblance 


236     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

of  the  three  enamel  tubercles  found  normally.     The  middle  tubercle, 
being  composed  of  defective  enamel,  is  soon  lost  by  abrasion,  causing 
the  tooth  to  have  a  notched  appearance  (Figs.  177,  178,  and  179). 
Black^  states  that  any  malnutrition,  even  a  burn,  typhoid  fever,  one 


Fig.  177 


Hutchinson's  teeth.     Hypoplasia.     Two  upper  centrals  notched  and  contracted.     Character- 
istically imdeveloped  upper  jaw.     From  an  hereditary  syphilitic,  aged  twelve  years. 

spasm,  etc.,  may  mark  teeth  as  a  nail  may  be  grooved.     He  claims  to 
have  seen  Hutchinson's^  teeth  without  history  of  taint. 

The  point  at  which  the  arrested  development  would  occur  is  that 
part   under  development  at    the  time  the  nutritional  disturbance 


Fig.  178 


Fig.  179 


.  S^«><«§ss^'^ 


Syphilitic  teeth  in  upper  and  lower  jaws  as 
they  appear  when  recently  erupted. 


The  teeth  of  hereditary  syphilis 
at  maturity. 


occurs.  Thus,  from  one  definite  attack  of  disease  the  centrals  are 
marked  nearer  the  neck  than  laterals,  and  these  nearer  than  cuspids. 
First  molars  are  often  occlusally  defective,  as  well  as  incisors; 
bicuspids  are  only  rarely  marked. 


I  Dental  Review,  1906. 


2  Dental  Digest,  1904. 


MACROSCOPIC  MALFORMATIONS  237 

A  lack  of  development  of  the  anterior  portion  of  the  upper  jaw  has 
been  noted  in  a  number  of  cases  clearly  syphilitic  (Fig.  172).  It  has 
been  noted  that  not  all  syphilitic  children  present  these  dental  appear- 
ances; and,  again,  appearances  said  to  be  identical  with  them  are 
observed  in  children  said  not  to  be  syphilitic;  nevertheless,  the  presence 
of  such  teeth  is  usually  regarded  as  a  valuable  diagnostic  sign  of 
hereditary  syphilis.  The  existence  of  interstitial  keratitis  and  of 
chronic  catarrh  of  the  middle  ear  in  connection  with  Hutchinson's  teeth 
are  held  to  be  positively  diagnostic  signs  of  hereditary  syphilis  (Hare). 

Therapeutics  based  upon  such  a  diagnosis  are  followed  by  better 
results,  as  a  rule,  than  when  the  general  indication  is  ignored.  The 
boy  from  whose  mouth  a  model  (Fig.  177)  was  obtained  had  interstitial 
keratitis  in  the  left  eye,  chronic  nasal  catarrh,  and  a  somewhat  flat 
development  of  the  nasal  bones. 

Tomes  favors  and  adduces  evidence  to  support  the  contention  of 
Hutchinson  that  honey-combed  incisal  edges  of  incisors  and  cuspids 
and  occlusal  surfaces  of  first  molars  are  indicative  of  mercurials 
administered  in  early  childhood. 

Pitted,  grooved,  or  otherwise  malformed  teeth  may  decay  sometimes 
so  badly  as  to  produce  a  black,  slimy  appearance  almost  loathsome 
to  view.     In  other  cases  surprisingly  little  caries  develops. 

Treatment. — If  slightly  pitted,  gold  or  porcelain  fillings  may  be 
introduced.  In  some  cases  grinding  off  the  rough  incisal  edge  is 
sufficient;  in  other  cases  the  teeth  may  require  to  be  drawn  down 
after  this  procedure,  or  porcelain  inlays  may  be  used  to  restore  the 
incisal  edges.  In  the  extremely  disagreeable  cases  above  mentioned 
some  form  of  crowning  must  be  resorted  to.  Fig.  180  exhibits  a 
restoration  of  the  case  shown  in  Fig.  175. 

Fusion  of  Teeth. — Two  or  more  teeth  may  be  united  during  the 
process  of  development.  The  union  may  occur  (1)  by  the  crowns, 
(2)  by  the  roots  alone,  and  (3)  by  both  crowns  and  roots. 

1.  Fused  teeth  united  by  the  crowns  alone  have  not  been  shown. 
The  nearest  approach  to  it  is  the  case  illustrated  by  Tomes,  in  which 
two  central  incisors  have  fused  by  union  of  the  crown  portions  and  one- 
fifth  of  the  root  portions  of  the  two  teeth  (Fig.  181).  Such  teeth 
would  have  dentine  common  to  both  crowns  at  the  point  of  union, 
the  enamel  being  reflected  over  the  outside  of  the  common  dentinal 
mass  according  to  the  scheme  shown  in  the  diagram  Fig.  185,  B.  The 
pulp  may  be  common  to  the  two  teeth  in  the  crown.  Of  course,  the 
root  pulps  are  separate 


238     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

The  condition  is  a  record  of  the  fact  that  prior  to  dentinification  the 
papillae  and  enamel  organs  of  the  two  teeth  have  coalesced  at  some 
point.  This  must  have  occurred  at  an  early  period,  perhaps  even 
during  the  descent  of  the  cords  into  the  jaw.  \\Tien  it  is  considered 
that  the  two  central  incisors  are  contained  in  two  separate  inter- 
maxillary bones,  the  rarity  of  such  a  union  and  in  such  a  manner 

Fig.  180 


Same  as  Fig.  171,  with  Land  jacket  crowns  placed  over  anterior  teeth.     (W.  A.  Capon.) 

may  be  appreciated.  I  have  seen  such  a  union  between  a  right  lower 
central  and  lateral  incisor  in  the  mouth.  Recession  of  the  gum 
permitted  a  view  of  the  cervical  conformation. 

2.  Those  teeth  united  by  fusion  of  the  roots  have  a  common  dentine 
at  the  point  of  union,  with  cementum  reflected  over  that.  The  pulp 
is  common  to  the  two  teeth  at  the  point  of  fusion. 


Fig.  181 


Lingual  view.  Labial  view. 

Fusion  of  two  permanent  upper  central  incisors  by  their  crowns  and  a  portion 

of  the  roots.    (Tomes.) 

In  the  specimen  shown  in  Fig.  182  at  a  there  is  but  one  apical 
foramen.  In  that  shown  at  b  and  c  there  is  but  one  foramen  for  the 
two  fused  portions  of  pulp,  though  the  other  canals  have  their  usual 
foramina.  These  cases  evidence  an  accidental  coalescence  of  pulps 
after  much  independent  root  formation. 

3.  Fusion  throughout  both  crowns  and  roots  have  the  same  charac- 


MACROSCOPIC  MALFORMATIONS 


239 


teristics  as  the  others  combined  in  the  one  specimen  (Figs.  186  and  187). 
The  diagram  (Fig.  185)  shows  the  scheme  for  the  crown  and  root. 


Fig.  182 


^ 


a,  fusion  of  two  molars  at  tlie  roots — two  pulp  cavities,  one  foramen;  b,  c,  fusion  of  super- 
numerary teeth  roots  to  buccal  roots  of  upper  molars,  pulp  canal  common  where  probes 
cross;  d,  view  of  resorbed  root  end  of  two  fused  temporary  teeth;  e,  concrescence  by  hyper- 
cementosis. 


Fig.  188  shows  specimens  of  fusion  in  both  the  upper  and  lower 
jaws.     It   occurs   also  with   the   temporary   teeth    (Fig.    189).     Fig. 


Fig.  183 


Attacliment  of  temporary  teeth  b.v  their 
pericemenfi. 

Fig.  184 


Fusion  of  a  supernumerary  tooth,  witli 
an  upper  third  molar. 


Fi.;.  185 


A ,  diagram  of  a  case  of  triple  fusion  show- 
ing crowns  with  independent  incisal  edges 
and  pulps,  but  otherwise  fused  into  one 
crown  with  one  pulp;  B,  transver.se  sec- 
tion of  same,  showing  common  pulp  cavity 
and  common  dentine  overlaid  by  enamel 
(or  cementum).  From  a  perfect  specimen 
in  the  editor's  collection. 


185,  A  shows  a  very  rare  condition,  the  fusion  of  the  temporary 
central,  lateral,  and  cuspid  of  one  side  (triple  fusion). 


240     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETWi 

Fusion  is  evidently  an  abnormality  of  development  dependent  upon 
coalescence  of  formative  organs  at  some  point,  and  is  most  likely  to 


Fig.  186 


Fig.  187 


Permanent  central  and  lateral  incisors  of  f»  Geminous  upper  laterals  with  common 
the  upper  jaw,  united  throughout  the  whole  pulp.  Practice  of  Dr.  Varney  Barnes, 
length  of  the  teeth.     (Tomes.)  (Skiagraph  by  E.  Ballard  Lodge.) 


occur  where  the  adjacent  tooth  follicles  have  least  anatomical  sepa- 
ration from  their  fellows.  The  roots  of  fused  temporary  teeth  are 
resorbed  as  usual  (Fig.  182,  d). 


Fig.  188 


A,  fusion  of  upper  geminou.s,  permanent  laterals;  B,  fusion  of  lower  right  permanent 
central  and  lateral  incisors.  , 

No  particular  treatment  is  required  unless  the  mass  in  some  way 
cause  interference  with  function,  which  is  unusual.  The  teeth  having 
a  common  pulp,  no  attempt  should  be  made  to  divide  them. 

Fusions  are  most  common  between  the  anterior  teeth  of  each  set 


MACROSCOPIC  MALFORMATIONS 


241 


and  between  the  second  and  third  or  third  and  fourth  (supernumerary) 
permanent  molars.  It  has  not  been  noted  in  bicuspids,  presumably 
because  these  teeth  lie  in  the  bifurcations  of  the  temporary  molars. 


Fig.  189 


Fig.  190 


Fusion  of  upper  temporary  teeth.     Double  fusion  of  lower  temporary  lateral  and  cuspid. 

Concrescence  of  Teeth. — Concresence  of  teeth  is  their  union  after 
the  tooth  is  formed;  it  is  evident,  therefore,  that  the  union  can  only  be 
caused  by  fusion  of  cementum.  This  means  that  during  the  formative 
and  eruptive  period  or  after  eruption  the  bony  partition  between  the 
teeth  disappears,  and  that  their  pericementi  be- 
come united,  receding  from  the  line  of  compres- 
sion as  cementum  is  deposited  between  and  joining 
the  roots.  The  united  teeth  show  evidences  of 
hypercementosis  at  points  other  than  the  point  of 
union  (Fig.  182,  e  and  Fig.  190).  At  times  the 
roots  of  the  same  tooth  undergo  either  fusion  or 
concrescence. 

During  the  eruption  of  the  third  molars,  par- 
ticularly the  upper,  temporary  lack  of  space  for 
the  eruption  of  the  crown  may  cause  resorption  of 
the  bone  covering  the  roots  of  the  second  molar, 
and  fusion  of  the  formative  pericementum  of  the  third  molar  with 
that  of  the  second  occurs;  a  deposition  of  cementum  then  binds  the 
teeth  together,  preventing  the  eruption  of  the  third  molar.  The 
lower  third  molar  rarely  presents  its  roots  to  those  of  the  second 
16 


Concrescence.  Third 
upper  mf>lar  impris- 
oned between  the  roots 
of  the  second  molar. 


242     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

molar;  the  contrary  presentation  is  the  rule.  The  condition  also 
occurs  apart  from  the  eruptive  process.  Excessive  hypercementosis 
upon  the  roots  of  individual  teeth  may  finally  result  in  their  union 
(Fig.  182,  e). 

In  at  least  one  case  the  crown  of  the  upper  third  molar  was  partly 
erupted  when  concrescence  occurred.  Retained  in  this  situation  the 
crown  decayed  away,  necessitating  extraction ;  the  second  molar 
came  away  with  it. 

The  only  treatment  required  for  concrescence  is  that  indicated  for 
impaction  or  hypercementosis  (which  see). 

Gemination  of  Teeth.  (Twin  Teeth.) — This  term  has  been  used 
by  Tomes  in  the  sense  of  union  of  teeth,  but  it  is  perhaps  better  used 


Pig.  191 


Double  gemination  of  upper  permanent  lateral  incisors. 

to  designate  supplemental  teeth  of  the  same  class.  In  twin  teeth  the 
enamel  organ  of  a  permanent  or  temporary  tooth  is  duplicated,  in  all 
probal)ility,  two  buds  arising  from  the  cord  or  band  as  the  case  maybe. 

Duplication  of  the  Pulp  Cavity. — Hopewell-Smith  calls  attention 
to  a  case  of  an  upper  permanent  central  incisor  containing  two  pulp 
cavities  in  the  coronal  portion,  probably  an  int(>rrupted  gemination. 

In  gemination  one  of  the  teeth  formed  is,  of  course,  a  supernu- 
merary tooth,  but  in  some  cases  both  are  typical  teeth  (Fig.  191). 
The  second  germ  may  develop  an  atypical  tooth  or  one  but  slightly 
abnormal  in  form.  The  geminous  teeth  may  undergo  fusion,  as  seen 
in  Fig.  188,  yl. 

Dilaceration  and  Flexion. — By  (h'laceration  is  meant  a  displacement 
of  a  formed  portion  of  a  tooth  in  such  a  manner  as  to  change  its 


MACROSCOPIC  MALFORMATIONS 


243 


relative  position  to  the  soft  parts  engaged  in  its  development,  the 
development  then  being  continued  in  the  new  relation.'  The  term 
"flexion"  may  be  made  to  include  cases  of  abnormal  development 
in  which  the  formative  tissues,  the  enamel  organ,  or  dentinal  papilla 
have  had  their  relative  positions  altered  by  unknown  forces.  If,  as  an 
example  of  dilaceration,  an  accident  to  a  temporary  tooth  occur, 
the  force  may  displace  the  partially  formed  permanent  crown.  The 
balance  of    the  crown    may   be  formed   in  the   new  situation  and 


Fig.  192 


PC 


Pulp  hernia  and  flexion,  mesiodistal  section: 
E,  enamel,  distal  section  in  the  bifurcation  of 
the  roots;  D,  dentine;  C  C,  cementum;  P  C, 
pulp  cavity:  F,  large  apical  foramen;  B  of  R, 
bifurcation  of  the  roots.  (From  a  specimen, 
enlarged.) 


be  of  fairly  perfect  or  of  imper- 
fect structure.  The  same  is  true 
of  the  tissues  of  the  root;  Fig. 
192  illustrates  both  conditions.- 
This  is  most  likely  to  occur  with 
the  anterior  teeth. 


Dilaceration.  Shows  fold  in  the  labial 
enamel  and  cervical  dentine.  (After  von 
Wunschheim.) 


As  an  example  of  flexion,  a 
portion  of  the  enamel  organ  of  a 
tooth  may  l)e  displaced  and  in 
its  new  relations  may  form  (Miaiiici  in  an  umi.sual  .situation,  as,  for 
example,  upon  the  side  or  luxk  of  the  root  (see  enamel  notlule)  or 
even  in  the  bifurcation  or  on  the  apex  of  the  root  (Fig.  193).  Again, 
it  is  probable  that  lack  of  space  may  cause  deflection  of  a  pulp 
engaged  in  root  formation,  a  curved  root  being  the  result  (Fig.  200). 
The  pericementum  (follicle  wall)  moves  with  the  pulj)  in  these  cases. 


*  Tomes. 

*  G.  von  Wunschheim,  Fracturen,  Infraktionen  und  Knickungen  der  Zahne. 


244     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


Unusual  Locations  of  Enamel. — That  during  development  the  enamel 
organ  or  portions  of  it  may  assume  an  abnormal  relation  to  the  pulp 
is  evidenced  by  odontomes.  Apart  from  these  there  are  evidences 
seen  in  teeth  which  show  that  portions  of  the  enamel  organ  may 
become  detached  from  the  main  organ  and  develop  enamel  in  unusual 
situations.  Thus,  columns  of  enamel  may  penetrate  the  body  of  the 
dentine. 


Fig.  194 


Fig.  195 


Enamel  excrescences. 

(Salter.) 


Lower  molar  with  enamel  nodule  connected  to  the 
enamel  of  crown  by  a  ridge  of  enamel. 


A  small  nodule  or  cap  of  enamel  overlying  dentine,  and  itself  over- 
lapped at  the  edges  by  cementum,  may  be  found  upon  the  root  of  a 
molar,  usually  upon  the  side  of  an  upper  third  molar  at  a  point  about 
one-eighth  inch  from  the  cervical  margin  of  the  crown  enamel;  but 
one  may  be  one-half  inch  distant  from  the  enamel  margin.  A  thin  ridge 
of   enamel   sometimes,  though   not  usually,  seen   connecting  them 


Fig.  196 


Fig.  197 


Fig.  198 


Fig.  196. — Upper  molar  with  supplemental  cu.sp  on  lingual  tide. 

Fig.  197. — Showing  unusual  development  of  the  cingule  or  basal  talon  on  an  incisor.     (From 
case  reported  by  W.  H.  Mitchell,  Dental  Co.smos,  vol.  xxxiv.) 
Fig.  198. — Very  large  supplemental  cusp  on  upper  molar. 


indicates  the  nodule  to  have  been  formed  by  a  detached  portion  of 
the  orginal  enamel  organ.  This  formation  is  known  as  an  enamel 
nodule.  It  may  occur  upon  a  lower  molar,  though  usually  found 
upon  the  upper  molars  (Fig.  195).  They  may  cause  neuralgia 
(Ottofy).  Two  may  exist  on  opposite  sides  of  a  molar,  as  in  a 
specimen  possessed  ))j  the  editor. 


MACROSCOPIC  MALFORMATIONS 


245 


A  molar  root  may  have  a  cap  of  enamel  upon  its  apex,  an  evidence 
of  extreme  displacement.  Sometimes  an  excrescence  may  be  found 
upon  the  enamel  (Fig.  194).  Fig.  193  shows  enamel  formed  in  the 
bifurcation  of  tlu>  roots  of  a  lower  molar. 

Supplemental  Cusps. — Occasionally  a  tooth  has  a  greater  numlier  of 
cusps  than  usual.  The  most  common  form  of  this  condition  is  a 
supplemental  mass  attached  to  the  palatal  side  of  the  mesopalatine 


I-io.  199 


Fig.  200 


Fig.  201 


Cu.spid.s  with  long  roots 


Curved  roots.  Upper  puspid  witli  two  roots. 


cone  of  the  upper  first  molars  (Fig.  19G).  It  is  more  rarely  the  case 
that  a  cingule  of  this  sort  is  noted  upon  the  lower  molars.  The  palatal 
tubercle,  the  prominence  upon  the  cingule  of  an  upper  incisor,  may  be 
of  exaggerated  size.  In  one  case  (Fig.  197)  this  development  gave  the 
appearance  of  a  talon  upon  the  tooth,  a  distinct  cusp  segment  in  itself. 


Fig.  202 


Fig.  203 


Fig.  204 


Short  buccal  root  of  a 
molar,  otherwise  properly 
developed. 


Central  incisor  with  short 
root. 


Five-rooted    upper  third 
molar. 


Fig.  198  illustrates  a  marked  supplemental  cusp  upon  the  buccal 
surface  of  a  molar. 

Malformations  of  Roots. — Ditterences  in  regard  to  the  size,  arrange- 
ment, form,  and  number  of  the  roots  of  teeth  are  the  most  common 
of  dental  malformations.  The  roots  of  teeth  may  be  abnormally  long 
(Fig.  199)  or  abnormally  short  (Figs.  202  and  203). 

The  roots  of  cuspids  may  be  bifurcated,  particularly  in  the  lower 


246     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


jaw  (Figs.  201  and  204).  A  central  may  have  a  short  supplemental 
root  (Guilford^. 

The  upper  first  bicuspids  may  have  trifurcated  roots,  the  extra  root 
usually  being  on  the  buccal  aspect.  The  upper  second  bicuspid  may 
be  bifurcated;  upper  molars  may  have  more  than  three  roots,  the 
third  molar  often  having  four,  five,  or  six,  and  in  one  case  reported 
eio-ht  roots  (Fig.  204).  In  some  cases  upper  third  molars  have  but 
one  root  with  a  single,  large  canal.  In  other  cases  the  roots  are  fused 
so  as  to  form  apparently  but  one  root,  while  the  canal  divisions  may 
exist.  Lower  molars  may  have  three  or  four  distinct  roots,  but 
rarely  only  one. 

Abnormalities  of  root  form  are  of  extreme  frequency,  and  are 
probably  explained  upon  the  hypothesis  of  flexion  of  the  root  pulp, 
previous  to  the  deposition  of  the  curved  portion  of  root  tissue. 


Fig.  205 


Fig.  206 


Fig.  207 


Fibrous  odontome.  (Gar- 
retson,  after  Peirce.) 


Two-rooted  lower  cu.spid.  Re- 
sorption of  temporary  roots.  (Skia- 
graph by  E.  Ballard  Lodge.) 


Results  of  hernia  of  a  pulp. 
(Salter.) 


It  is  impo.ssible  to  diagnosticate  the  forms  of  roots  from  the  appear- 
ance of  the  crowns,  but  a  skiagraph  will  determine  their  form  with 
certainty.  It  may  be  said,  however,  that  narrow  necks  indicate  a 
probable  divergence  of  roots,  and  vice  versa. 

Odontomata. — An  odontoma  is  a  growth  composed  of  structures  of 
which  the  teeth  are  composed,  but  the  masses  may  be  so  arranged 
as  to  have  no  typical  form  or  even  resemblance  to  a  tooth.  They  may 
appear  in  the  arch  or  may  remain  embedded  in  the  jaw,  where  they 
may  lie  quiescent  or  may  excite  cyst  formation  (Fig.  31),  or  give  rise 
to  various  morbid  reactions,  such  as  tumor  formation. 


>  American  System  of  Dentistry. 


MACROSCOPIC  MALFORMATIONS 


247 


It  has  been  held  by  Broca  that  any  of  the  formative  organs  of  the 
tooth — enamel  organ,  dentinal  papilla,  or  follicle  wall — may  undergo 
aberrant  development  and  may  thereafter  deposit  calcific  tissue  or 
not,  as  the  case  may  be.  If  not,  soft  tumors  of  the  jaw  not  distinctly 
dental  may  form,  though  in  its  complete  form  such  a  tumor  may 
l)ecome  a  seat  of  calcific  deposition  peculiar  to  the  aberrant  tissue. 
Bland-Sutton's  classification  is  usually  adopted,  and  is  as  follows: 
1.  Aberrations  of  the  Enamel  Organ:  (a)  Epithelial  otlon tomes. 
(h)  Calcified  epithelial  od  on  tomes. 

Fig.  208 


Fig.  207  magnified. 


2.  Aberrations  of  the  Follicle:  (a)  Follicular  cysts.  (b)  Fibrous 
odontomes.     (c)  Cementomata.     {d)  Compound  follicular  odontomes. 

3.  Aberrations  of  the  Papilla:  (a)  Radicular  odontomes.  (6) 
Dentomata.     (c)  Osteodentomata.     (d)  Cementomata. 

4.  Aberrations  of  the  Whole  Tooth  Germ  (or  three  formative 
organs),  Composite  Odontomes. 

The  Uncalcified  Odontomata:  1.  Epithelial  odontomata  which 
arise  by  aberrant  development  of  the  enamel  organ,  and  remaining 
uncalcified  resemble  the  adenomata. 


248     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


2.  Follicular  Odontomata :  (a)  The  wall  of  the  follicle  is  distended 
and  the  cavity  is  filled  with  a  thick  fluid  (sometimes  pus  if  infected) 
and  contains  a  portion  of  imperfectly  developed  tooth.  It  is  in  this 
form  really  a  cyst  (Fig.  31).     (&)  The  follicle  wall  or  pericementum 


Fig.  209 


Fig.  210 


Radicle  or  odontome.      (Tomes.) 


Odontoma.     (Garretson.) 


may  thicken  so  as  to  form  a  fibrous  capsule  about  the  tooth  suf- 
ficiently resistant  to  prevent  its  eruption  (Fig.  205).  This  is  called 
a  fibrous  odontome. 

3.  Compound  Follicular  Odontomata:  The  follicle  wall  thickens 
into  a  fibrous  capsule,  and  in  this  may  appear  fragments  of  cementum, 


Fig.  211 


Composite  odontome.      (Garretson.) 

dentine,  or  imperfectly  formed  teeth  with  their  enamel,  dentine,  and 
cementum. 

It  is  a  combination  of  an  uncalcified  and  calcified  form,  and  might 
easily  lead  to  formation  of  a  cyst  containing  many  teeth  or  portions 
of  teeth. 


MACROSCOPIC  MALFORMATIONS 


249 


The  Calcified  Odontomata:  1.  Epithelial.  The  enamel  organ 
develops  aberrantly  into  a  large,  possibly  multilocular  mass,  and 
enamel  deposition  occurs. 

2.  The  Cementomata:  A  fibrous  odon tome  forms  from  the  follicle 
wall,  then  calcifies  into  laminated  ossific  material.  One  from  a 
horse,  in  the  Royal  Veterinary  College,  London,  weighed  seventy 
ounces.     It  may  include  one  or  more  teeth. 

3.  Radicular  Odontomata:  The  crown  may  form  normally,  but 
the  dentinal  papilla  becomes  aberrant  and  develops  largely,  conveying 
with  it  the  follicle  wall.  Ceasing  to  enlarge,  cementum  and  dentine 
are  deposited  somewhat  in  the  ordinary  manner,  but  of  somewhat 
aberrant  deposition.  Pulp  hernia  comes  under  this  heading  and  acts 
similarly  (Figs.  207,  208,  and  209). 

Fig.  212 


Composite  odontome. 

4.  Composite  Odontomata:  The  developmental  organs,  the  enamel 
organ,  the  papilla,  and  follicle  wall  are  aberrant,  heterogeneously 
arranged,  enlarged,  and  then  deposit  a  composite  mass,  which  may  be 
somewhat  orderly  and  tooth-like  (Fig.  210),  or  be  totally  unlike  a 
tooth  as  in  Figs.  211  and  212. 

Treatment. — The  treatment  of  odontomata  is  usually  that  directed 
to  their  sequels,  and,  as  a  rule,  involves  their  removal  by  surgical 
operation. 

Anomalies  of  Number. — Although  the  dental  series  of  man 
normally  consists  of  thirty-two  members,  cases  are  frequently  observed 
in  which  the  number  is  less  than  or  in  excess  of  that  number. 

Deficiency. — It  is  observed  with  some  frequency  that  the  upper 
lateral  incisors  never  make  their  appearance,  a  condition  traceable  to 


250     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

the  influence  of  heredity  in  some  of  the  instances.  In  an  interesting 
case  of  three  sisters,  who  all  were  without  upper  laterals,  a  son  of  one 
of  them  had  them.  Unfortunately  the  history,  as  to  the  parents  of 
the  sisters,  was  not  certain,  as  they  wore  artificial  teeth. 

\Mien  the  laterals  are  absent  the  permanent  cuspid  erupts  and 
occupies  the  lateral  incisor  space,  and  thus  sometimes  fails  to  cause 
resorption  of  the  root  of  the  temporary  cuspid,  which  persists  in  the 
cuspid  space.  The  lower  laterals  sometimes,  but  more  rarely,  fail 
to  appear;  are  probably  never  formed.  The  third  molar  may  never 
appear,  or  appear  as  a  peg-like  tooth. 

The  cases  of  suppressed  teeth,  next  in  point  of  frequency,  are  those 
of  the  bicuspid  teeth.     If  the  corresponding  teeth  are  all  present  in 

Fig.  213 


Structure  of  a  composite  odontome. 

the  dental  arch,  a  well-founded  suspicion  of  impaction  of  the  missing 
tooth  may  be  entertained. 

An  excessive  growth  of  hair  upon  the  face  and  body  has  also  been 
associated,  in  some  cases,  with  a  deficiency  in  number  and  alteration 
in  form  of  the  teeth.  '  In  other  cases  no  abnormality  was  noticeable.^ 
In  some  cases  the  hair  and  other  dermal  structures  may  be  normal 
and  the  teeth  be  quite  deficient  in  number. 

The  extreme  of  suppressed  formation  is  represented  in  a  case 
described  by  Guilford.^ 

A  patient  over  fifty  years  old  had  never  erupted  any  teeth,  temporary 


'  Tomes. 


^  American  System  of  Dentiijtry,  vol.  iii. 


MACROSCOPIC  MALFORMATIONS 


251 


or  permanent;  the  alveolar  arches  revealed  no  evidences  of  enclosed 
teeth,  but  had  the  appearance  of  typical  edentulous  jaws;  the  alveolar 
bone  itself  was  but  primitive.  The  case  appeared  to  be  sporadically 
hereditar}',  a  grandparent  and  an  uncle  exhibiting  a  like  condition. 
The  cases  are  interesting  also  because  of  additional  evidences  of  faulty 
evolution  of  dermoid  structures.  In  the  first  case  cited  no  sudorip- 
arous glands  appear  to  have  formed,  and  there  was  but  a  faint  growth 
of  hair  on  the  cranium,  and  none  on  the  face  and  body.  The  uncle 
was  hairless  and  edentulous  from  birth.  Guilford  found,  in  other 
members  of  the  family,  an  absence  of  the  full  eomi)lemeiit  of  teeth. 

In  an  interesting  summary,  Kjaer^  quotes  Trueswell  as  knowing  of  a 
man,  aged  fifty-four  years,  having  had  no  permanent  teeth,  but  all  of 


Fig.  214 


Malposition  of  molar  germs. 

his  temporary  ones,  and  Fricke  as  having  three  cases  of  retention  of 
temporary  teeth  until  sixteen,  eighteen,  and  twenty  years,  respectively, 
when  the  permanent  teeth  ap})eare(l,  and  Linderer  as  having  a  case 
of  a  lady,  aged  sixty  years,  who  never  had  any  teeth,  and  a  case  of  his 
own  in  which  the  temporary  teeth  were  lost  from  time  to  time,  but 
no  permanent  successors  appeared  and  none  could  be  detected  by 
skiagraphy.  He  attributed  the  lack  to  some  disturbance  during 
fetal  life,  as  the  family  history  did  not  include  such  a  case. 

Excess. — ^The  possible  occurrence  of  a  condition  in  some  respects 
the  reverse  of  the  preceding  has  been  much  written  of  and  discussed 
— i.  e.,  the  occurrence  of  a  complete  third  denture.     There  can  be  but 


»  Dental  Cosmos.  1907. 


252     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

one  conclusion  from  an  examination  of  all  the  evidence  thus  far 
presented,  and  that  is  that  no  clear  and  well-authenticated  cases  are 
made  out.  Isolated  cases  of  the  appearance  of  teeth  subsequent  to 
the  loss  of  all  of  the  second  denture  are  not  infrequent;  and,  so  far  as 
clear  records  can  be  obtained,  are  resolvable  into  cases  of  the  eruption 
of  supernumerary  or  impacted  teeth.  While  these  cases  are,  at  least 
for  the  present,  to  be  held  as  unproved  in  connection  with  elderly 
persons,  a  well-authenticated  case  of  multiple  dentition  in  a  child 
is  recorded  by  Catching.^  Between  the  sixth  and  seventh  month  the 
eruption  of  one  set  of  teeth  was  complete;  within  three  months  all  of 
these  had  been  lost.  Between  the  eleventh  and  fifteeth  months 
another  period  of  dentition  occurred,  the  teeth  of  this  second  denture 
being  of  such  faulty  structure  as  to  crumble  away  quickly.  At  the 
age  of  two  and  one-half  years  a  third  dentition  appeared,  which  caused 
the  child  such  inconvenience  that  the  teeth  were  extracted  by  the 
mother.  At  the  age  of  eleven  years  a  fourth  series  erupted,  incom- 
plete through  the  absence  of  six  teeth.  At  the  age  of  fifteen  these 
teeth  were  sound  and  firm. 

Fourth  Molar. — The  molar  series  of  man,  particularly  in  the  lower 
negroid  races,  may  consist  of  four  instead  of  three  members.  When 
the  fourth  molar  appears  in  the  white  races  it  is  usually  as  a  stunted 
member,  a  conical  or  peg-like  tooth,  similar  to  that  which  occasionally 
replaces  the  third  molar.  There  is  rarely  room  posterior  to  the  distal 
wall  of  the  third  molar  for  their  eruption,  so  that  they  usually  make 
their  appearance  in  the  region  shown  in  the  illustration.  S.  M. 
Hartman,^  L.D.S.,  of  Victoria,  B.  C,  has  furnished  the  model  (Fig. 
215)  of  a  case  in  which  the  molar  form  of  the  fourth  tooth  is 
unusually  well  pronounced. 

Supernumerary  Teeth. — Any  teeth  in  excess  of  the  noimal  thirty- 
two,  although  clearly  cases  of  reversion  of  type  in  many  instances,' 
are  included  in  the  category  of  supernumerary  teeth.  Supernumerary 
teeth  appear  as  simple  unmodified  cones,  or  as  combinations  of  cones 
resembling  the  forms  of  teeth.  The  conical  form  is  most  common. 
Cases  where  these  peg-like  teeth  appear  around  the  third  molars, 
singly  or  in  number,  are  numerous.  Their  appearance  in  any  situa- 
tion is  evidence  that  the  normal  number  of  dental  cords  has  been 
exceeded.  They  are,  perhaps,  all  to  be  regarded  as  cases  of  long  rever- 
sion, not  alone  because  they  increase  the  number  of  the  dental  series, 

'  Southern  Dental  .Journal,  October,  1886.  ^  Dental  Cosmos,  1891. 

'  A.  H.  Thompson,  American  System  of  Dentistry,  vol.  iii,  and  American  Text-book  of 
Operative  Dentistry. 


MACROSCOPIC  MALFORMATIONS 


253 


but  because  they  have  primitive  forms,  a  modification  of  the  forms 
found  among  the  reptiles  and  fishes. 

Guilford^  divides  supernumerary  teeth  into  those  having  typical 
anatomical  forms  and  those  having  atypical  forms. 


Fig.  215 


The  fourth  molar.     (Hartman.) 
Fig.  216 


Two  atypical  upper  supernumerary  teeth  displacing  the  inci.«ors. 

Supernumerary  incisors  having  typical  forms  appear  in  either  jaw. 
In  the  upper  jaw  .supernumerary  centrals  and  laterals  both  appear, 

'  American  Sj'stem  of  Dentistry,  vol.  iii. 


Fig.  217 


254     MALPOSITIONS  AND  MALFORMATIONS  OF  THE  TEETH 

the  latter  more  frequently  (Fig.  191).  Supernumerary  teeth  may 
occupy  any  position  relative  to  the  dental  arch,  but  are  more  frequently 
seen  at  its  lingual  side.  The  compound  cone  occasionally  appears 
(Fig.  217).  In  addition  to  molars  and  incisors,  supernumerary 
bicuspids  are  occasionally  found  (Fig.  218);  super- 
numerary cuspids  are  very  rare,  but  sometimes  a 
brood  of  them  exists,  as  many  as  seventeen  fairly 
defined  small  teeth  having  been  removed  from  a 
cyst  in  the  location  of  the  cuspid  tooth.^ 

Unless   supernumerary    teeth    are   a    source   of 
offence,  either  through   their  position  or   appear- 
ance, they   need   not   be  disturbed.      If   they   are 
found  to  be  so,  they  may  be  extracted. 
Malpositions  of  the  Teeth. — A  tooth  is  said  to  be  in  malposition 
when  it  is  not  in  normal  relation  with  the  dental  arch  to  which  it 
belongs  and  to  its  antagonizing  teeth  of  the  opposing  arch.     Teeth  are 
found  in  abnormal  positions  as  the  result  of  a  variety  of  causes.     Some 


The  compound  cone. 


Fig.  218 


Case  of  seven  lower  bicuspids,  two  supernumeraries  in  place  and  one  erupting.  This  patient 
has  two  supernumerary  upper  central  incisors  displacing  the  centrals  proper,  yet  closely 
resembling  them. 

of  these  operate  prior  to,  during,  or  immediately  after  eruption;  some 
long  after  the  eruption  of  the  teeth,  and  some  because  of  non-eruption 
of  teeth.     (See  p.  211.) 


'  D.  M.  Clapp,  International  Dental  Journal,  1900. 


MACROSCOPIC  MALFORMATIONS  255 

Malpositions  which  are  remediable  through  the  application  of 
mechanical  force,  applied  by  means  of  suitable  apparatus,  belong  to 
operative  dentistry,  as  has  been  stated.  They  are  fully  treated  of  in 
works  upon  operative  dentistry^  and  orthodontia.^ 

The  extraction  of  teeth  after  they  have  been  erupted,  or  of 
their  predecessors,  is  one  of  the  most  frequent  causes  of  acquired 
malposition  of  the  remaining  teeth.  The  teeth  move  from  their 
original  positions,  the  anterior  teeth,  incisors,  laterals,  cuspids, 
and,  occasionally,  the  bicuspids  having  a  tendency  to  drift  poste- 
riorly, sometimes  opening  a  space  between  the  central  incisors 
sufficiently  large  to  create  a  deformity.  The  molars  have  a  decided 
natural  tendency  to  drift  foward,  and  when  the  bicuspids  are  removed 
they  tip  anteriorly,  causing  malocclusion  upon  their  distal  cusps  and 
sometimes  their  distobuccal  cusps  alone,  with  a  further 
tendency  to  tip  forward  and  sometimes  inward  as  well.  fig.  219 

Separation  of  the  posterior  teeth  may  occur,  and  in  any 
event  the  loss  of  mesial  or  distal  support  permits  fibrous 
food  to  be  packed  between  the  teeth;  as  they  spring 
slightly  apart,  it  is  held  by  their  springing  together 
again.    The  lack  of  occlusion  brought  about  by  extrac- 
tion of  antagonists  permits  elongation,  and  the  loss  of 
posterior  support  is  apt  to  bring  about  labial  protrusion 
or  abrasion  of  upper  anterior  teeth.     This  effect  is  pro- 
duced in  youth  when  the  first  molars  are  lost  before  the 
bicuspids  are  in  place  (Fig.  219).    The  first  molars  are      Kffectsof  prema- 
the  keystones  of  the  arches,  and  determine  the  extent  of    ,,3^  g,.st  molars, 
the  formative  process  which  shall  occur  in  the  alveolar 
bone  posterior  to  them.     They  are  also  the  teeth  which,  correctly 
placed  or  out  of  position,  determine  the  occlusion  of  the  teeth. ^ 

If  a  temporary  tooth  be  long  retained,  it  is  sometimes  raised  to  the 
occlusal  level  of  the  other  teeth;  again,  it  is  sometimes  left  at  its  original 
level  and  occasionally  imprisoned  between  other  teeth.  The  x-ray 
should  be  used  to  determine  the  presence  or  absence  of  the  permanent 
tooth  germ  or  resorption  of  the  temporary  roots. 

If  teeth  erupt  in  malposition,  it  is  held  to  be  wise  to  correct  as  early 
as  possible,  in  order  to  prevent  further  malposition  of  other  teeth. 

Fig.  214  illustrates  a  case  of  malposition  of  molar  germs  which 
have  developed  in  the  incisal  region,  displacing  the  incisors. 

'  American  Text-book  of  Operative  Dentistry.  '  Guilford,  .\ngle,  and  others. 

'  Angle. 


256     MALFORMATIONS  AXD  MALPOSITIONS  OF  THE  TEETH 

Impacted  and  Encysted  Teeth. — The  extreme  extent  of  dental 
malposition  is  reached  when  the  permanent  teeth  do  not  erupt  at  all. 
Instead  of  presenting  in  the  dental  arch,  they  may  be  entirely  embedded 
in  the  substance  of  the  bone,  either  remaining  there,  with  or  without 
pathological  manifestations,  or  erupting  in  some  unusual  situation. 
In  other  cases  a  distinct  cystic  tumor  forms  about  the  enclosed  tooth 
(Fig.  31). 

Impacted  Lower  Third  Molars. — By  far  the  most  common  dental 
impaction  is  that  of  the  lower  third  molar.  The  extent  of  impaction 
varies  from  a  partial  eruption,  or  partial  imprisonment  of  the  tooth  by 
its  bony  surroundings,  to  its  entire  imprisonment  in  any  part  of  the 
ramus.     Many  of  the  more  severe  cases  treated,  under  the  head  of 

Fig.  220 


Right  half  of  lower  jaw,  showing  an  impacted  third  molar.      (Cryer.) 

difficult  eruption,  if  unrelieved,  would  be  included  in  the  category  of 
impacted  teeth. 

In  Fig.  220  is  shown  a  lower  third  molar  presenting  the  effects  of  a 
previous  impaction.  The  irritation  caused  by  the  efforts  of  the  tooth  to 
disengage  itself  or  to  overcome  the  resistance  to  its  eruption  has  caused 
an  active  formative  reaction  in  the  pericementum,  resulting  in  an 
hypertrophy  of  the  cementum. 

If  the  distance  between  the  posterior  surface  of  the  second  molar 
and  the  columns  of  the  coronoid  process  be  very  short,  it  is  evident  that 
upward  eruption  is  impossible,  so  that  the  tooth  may  assume  any 
flirection  of  movement,  the  most  common  being  forward,  the  axis  of 
the  tooth  changing  its  position  until  the  tooth  may  lie  in  a  horizontal 
position  or  even  become  inverted. 


MACROSCOPIC  MALFORMATIONS 


257 


Fig.  221  is  taken  from  the  same  jaw  as  Fig.  220,  but  shows  the 
opposite  side;  the  impaction  is  pronounced.  Fig.  222  shows  another 
case  with  different  anatomical  surroundings.     In  the  first  case  there 


Fig.  221 


Inner  side  of  left  half  of  same  lower  jaw.      (Cryer.) 
Fig.  222 


Impaction  of  lower  thii  J  nii.lai.     lit-Miiiiiiwn  .ii  mmii  i.i  .sftiiini  mulur  and  impingement 
of  root  upon  inferior  dental  canal,  which  is  deflected  out  of  its  course.     (Cryer.) 


were  evidences,  both  in  the  tooth,  in  its  bony  surroundings,  and  in 
the  external  cortical  bone,  of  the  resuhs  of  the  irritation  produced  by 
the  efforts  at  eruption.     The  cementum  was  thickened;  the  outer 


Fig.  223 


258     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

follicular  wall,  the  tissue  designed  to  form  the  alveolar  periosteum,  had 
exercised  its  formative  osteogenetic  function,  and  a  capsule  of  bone  had 
formed  about  the  tooth;  it  lay  in  a  bony  chamber.  The  pressure 
exerted  upon  the  distal  wall  of  the  second  molar  had  resulted  in  a 

pressure  resorption  of  its  root  until 
the  pulp  chamber  was  encroached 
upon.  These  were  both  postmor- 
tem cases,  and  no  records  of  their 
clinical  histories  were  obtainable. 
The  symptoms  produced  could  only 
be  surmised  by  the  nature  of  the 
anatomical  relations  and  the  patho- 
logical evidences.  There  may  have 
been  a  prolonged  but  mild  perios- 
titis, probably  a  continued  pulp 
irritation ;  and  in  the  last,  neural- 
gia of  any  grade  of  severity. 
Judging  from  postmortem  records  and  recent  skiagraphy,  cases  of 
impacted  third  molars  are  more  common  than  generally  believed. 
Instead  of  remaining  in  the  alveolar  portion  of  the  bone,  the 
impacted  tooth  may  come  to  occupy  a  cavity  in  some  portion  of  the 
body  or  the  ramus  of  the  bone  (Figs.  226  to  229).     The  positions  of 

Fig.  224 


Impacted  lower  third  molar  beneath  gum. 
Second  molar  tipped  forward.  (Skiagraph 
byJE.  Ballard  Lodge.) 


Impacted  cuspid.      (Skiagraph  l)y 
E.  Ballard  Lodge.) 


Impacted  bicuspid.      (Skiagraph  by  E 
Ballard  Lodge.) 


the  teeth  in  such  cases  tend  to  confirm  Tomes'  theory  of  the  develop- 
ment of  the  jaw.  The  jaw  being  lengthened,  and  the  ramus  develop- 
ing through  conjoined  deposition  and  resorption  of  bone,  the  crown 
of    the   tooth   appears   to  be  either   fixed   in  a  bony  nucleus  and 


MACROSCOPIC  MALFORMATIONS 


259 


transported  to  some  distant  point  in  the  developmental  progress  of 
the  jaw,  or  to  be  irregularly  shifted  about  during  jaw  growth.  At 
later  periods  the  pressure  exercised    by  root  formation  disturbs  the 


Fig.  225 


Same  as  shown  in  Fig.  221,  witli  tooth  removed.     (Cryer.) 

relations  of  the  tooth  with  its  earlier  surroinidings.  These  ell'orts  at 
eruption  may  at  late  periods  cause  the  appearance  of  the  tooth  in 
odd    situations.     In  the  case  shown    in   Fii;.  22.S    the  crown  of   the 


Fig.  226 


Wisdom  teeth  embedded  in  the  rami  of  the  lower  jaw.     (Tomes.) 

tooth  made  its  way  through  the  angle  of  the  bone  and  through  the 
muscles  and  skin.  The  opening  in  the  skin  healed  upon  extraction 
of  the  tooth. 


260     MALFORMATIONS  AXD  MALPOSITIONS  OF  THE  TEETH 


Fig.  227 


Impacted  Upper  Third  Molars. — Some  phases  of  impaction  of  this 
tooth  have  been  spoken  of  under  the  head  of  Pathological  Dentition. 

The  most  common  is  imprisonment 
of  the  tooth  and  its  subsequent 
partial  eruption  in  a  horizontal  posi- 
tion, the  crown  pointing  toward 
the  cheek  (Fig.  157).  The  crown 
of  this  tooth  may,  in  rare  cases,  be 
directed  inward  or  backward,  in  the 
latter  case  being  arrested  by  the 
pterygoid  plates  of  the  sphenoid 
bone.  It  may  present  with  an 
anterobuccal  facing  of  the  crown, 
as  shown  in  Fig.  229,  or  with  a 
posterobuccal  facing. 

In   a  case  recorded   by   Tomes 

(Fig.    230)    the   extraction   of    the 

second    molar   revealed    the  third 

molar  in  a    reversed    position,  its 

roots    occupying     the     depression 

between   the   roots  of   the  second 

molar.    A  case  has  been  reported  of  an  upper  molar  with  the  roots 

partly  embedded  in  the  floor  of  the  antrum,  its  neck  carious,^  and  the 

antrum  in  a  state  of  suppuration. 

Impacted  Cuspids. — In  point  of  frequency  of   impaction  the  upper 
cuspids  stand  next  to  the  lower  third  molars.     It  will  be  recalled  that 


Wisdom  tooth  buried  in  the  ramus 
(Tomes,  after  Marshall.) 


Fig.  228 


From  a  wax  model  in  the  museum  of  tlie  IjoikIdh  Odontological  Society.     (Tomes.) 

the  upper  cuspids  lie  high  up;  the  floors  of  their  crypts,  in  which  they 
lie  loosely,  are  at  a  higher  level  than  those  of  the  adjoining  teeth;  they 


'  Possibly  resorbed  or  decalcified  instead  of  carious.      (Editor.) 


MACROSCOPIC  MALFORMATIONS 


261 


erupt  at  a  much  later  period,  and  their  crowns,  as  with  the'other 
anterior  teeth.  He  h'ngual  to  the  roots  of  their  predecessors.  All  of  these 
are  elements  which  might  cause  displacement  of  the  developing  cuspids. 


Fig.  229 


Fig.  230 


A  second  molar  of  the  upper  jaw,  with  the 
wisdom  tooth  inverted  and  embraced  within 
the  roots.     (Tomes.) 


Upper  jaw,  with  the  third  molar  directed 
forward  and  impinging  upon  the  second  molar. 
The  small  tooth  situated  high  up  in  tlie  ante- 
rior part  of  the  jaw  was  forced  there  by  tlie 
spade  of  the  grave-digger.  The  artist's  accu- 
racy in  delineating  all  parts  of  the  specimen  has 
rendered  this  explanation  necessary.     (Tomes.) 


Should  the  advance  of  eruption 
not  keep  pace  with  the  develop- 
ment of  the  alveolar  bone,  im- 
prisonment is  likely;   again,  the 
dense   bone    immediately   about 
the  first  bicuspid  and  lateral  incisor  may  offer  a  deflecting  resistance. 
Examining  the  texture  of  the  bone  about  these  parts,  it  is  evident  that 
the  direction  of  least  resistance  to  the  advance  of  a  much  deflected 

Fig.  231 


Abnormal  jaw,  showing  impacted  cuspids.     (Cryer.) 

crown  is  into  the  cancellated  bone  of  the  incisor  portion  of  the 
alveolar  process;  hence  it  is  most  usual  to  find  the  crowns  of  these 
teeth   lying  with  their  cusps  pointing  forward  (Figs.  223  and  231). 


262     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

Several  recorded  cases  have  the  positions  shown;  one  or  both  of  the 
teeth  may  be  impacted.      Cuspid  teeth  may  erupt  into  the  nasal 

Fig.  232 


Impacted  bicuspid.     (Salter.) 


cavity,  appear  in  the  canine  fossa,  and  present  the  crowns  cheekwise 
or  lie  horizontally  and  above  the  roots  of  the  bicuspids. 

Glas,^  of  Vienna,  discovered  a  cuspid  in  the  nasal  floor  associated 
with  calcic  formations   in   its   ulcerated   surface    (rhinolith).     The 


Fig.  233 


Lower  maxilla,  in  which  the  right  second  Vjicuspiil  ]-  jihiciil  obliquely,  the  root  being  directed 
backward.  The  crown,  Miougli  exposed,  does  not  rise  above  the  level  of  the  alveolar  margin. 
(Tomes.) 

patient,  aged  nineteen  years,  had  frequent  fetid  eructations,  with  vomit- 
ing of  green,  foul-smelling  masses.  With  the  removal  of  the  cuspid  the 
vomiting,  etc.,  ceased. 

1  Dental  Surgery,  1907. 


MACROSCOPIC  MALFORMATIONS 


263 


Impaction  of  Other  Teeth. — While  impactions  are  most  common  in 
connection  with  the  teeth  named,  any  other  teeth  of  a  denture  may 
be  imprisoned.     Fig.  232  shows  an  impacted  bicuspid  whose  root 


Fig.  234 


Imprisoned  central  inci.^nr.      (Kirk  and  Cryer. 


development  has  l)een  normal  as  regards  its  length,  but  whose  curve 
has  been  modified  by  the  resistance  of  surrounding  tissues.  Fig.  234 
(see  also  Fig.  224)  exhibits  an  imprisoned  central  incisor,  whose 
retention  was,  no  doulit,  determined  and  malposition  caused  by  the 


Fic.  235 


Maxilla,  in  which  the  temporary  cuspids  (the  sockets  of  which  are  shown  by  the  dotted  lines) 
were  retained,  and  the  permanent  canines  developed  within  the  substance  of  the  jaw.  The 
bone  has  been  removed  on  the  one  side  to  show  the  direction  taken  by  the  tooth,  which  has 
been  twisted  on  its  axis  to  the  extent  of  a  quarter  of  a  turn.     (Tomes.) 


development  and  presence  of  the  brood  of  supermimerary  teeth  which 
surrounded  its  crown. 

Upper  incisor  teeth  have  been  seen   inverted   and   their  crowns 


264     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

erupted  into  the  nasal  cavity,  where  they  have  produced  inflammation 
which  later  became  infective/ 

Symptoms. — The  most  common  symptom  attendant  upon  impaction 
of  teeth,  judging  from  the  obtainable  records  of  cases,  is  trifacial 
neuralgia  of  any  degree,  caused  by  impingement  of  the  malposed  tooth 
upon  nerve  filaments  or  trunks.  Cryer^  records  a  case  where  a  supra- 
maxillary  neuralgia  was  traced  to  the  presence  of  a  central  and  lateral 
incisor  and  a  cuspid  tooth  in  the  anterior  wall  of  the  antrum;  they 
were  only  discovered  by  an  exploratory  operation  (Fig.  236).  A  cure 
of  the  neuralgia  was  effected  by  their  removal. 

Impacted  third  molars  frequently  give  rise  to  heavy  rheumatic  pains 
about  the  side  of  the  face  and  jaws,  and  no  doubt  in  such  cases  as 
depicted  in  Fig.  222  would  cause  intractable  and  diffuse  maxillary 
neuralgia.  Salter^  records  a  case  of  long  standing  and  intractable 
neuralgia,  exhibiting  a  constant  painful  area  upon  the  scalp,  and  in 
which  heat  and  tenderness  were  noticed  over 
Fig.  236  ^  Swelling  upon  the  hard  palate.     Immediate 

and  permanent  cessation  of  the  neuralgia  fol- 
lowed removal  of  the  teeth. 

Symptoms  of  maxillary  periostitis — heavy, 

gnawing,  and  dull,  throbbing  pain,  with  more 

or  less  heat  and  engorgement  of  tissues — are 

noted  as  an  accompaniment  of  impacted  teeth. 

Such  symptoms  may  herald  the  appearance  of  the  tip  of  the  tooth 

through  its  bony  covering  and  gum. 

Cases  of  maxillary  abscess,  in  the  absence  of  their  usual  cause 
(gangrenous  pulp),  may  run  a  prolonged  and  painful  course,^  involving 
neighboring  structures,  and  after  free  venting  be  found  to  have  arisen 
about  an  impacted  tooth. 

Occasionally  a  circumscribed  swelling  is  noted  upon  some  aspect  of  a 
jaw,  most  frequently  upon  the  palatal  portion  of  the  superior  maxilla, 
which  is  attended  by  inflammatory  symptoms,  and  an  incision  reveals 
an  impacted  tooth. 

Quickly  forming  cysts  of  the  jaw,  upon  receiving  surgical  treatment, 

may  be  found  to  contain  the  crown  of  an  entire  tooth,  this  evidently 

being  the  centre  of  irritation  from  which  the  cystic  formation  had  its 

origin. 

The  pulps  of  other  teeth  have  been  devitalized  by  the  strangulation 

'  Jameson,  International  Dental  Journal,  1899.  ^  Dental  Cosmos,  1896. 

'  Dental  PatholoKy. 

*  See  Garretson's  Oral  Surgery  and  Salter's  Dental  Pathology. 


MACROSCOPIC  MALFORMATIONS  265 

due  to  the  pressure  of  the  crown  of  the  impacted  tooth  upon  the  apical 
tissue,  and  the  production  of  pulp  nodules  in  other  teeth  through  a 
reflex  hyperemia  has  been  noted.  The  resorption  of  roots  of  other 
teeth  has  been  produced  by  the  pressure  of  the  impacted  tooth. 

Hypercementosis  and  concrescence  have  also  been  produced  by  the 
descent  of  the  tooth  and  have  produced  impaction. 

Resorption  of  the  roots  of  the  impacted  teeth,  or  resorption  of  the 
enamel  and  dentine  of  the  crown  may  occur.     In  one  case  a  calculus  in 
no  wise  associated  with  the  oral  cavity  and  divided  from  it  by  an 
area  of  pericemental  tissue  was  found.    (See 
Resorption  of  Enamel  for  illustration.)     Even  Fig.  237 

dementia  has  been  associated  with  impaction. 

In  all  these  cases  diagnostic  features  exist, 
though  none  are  comparable  to  the  a;-rays. 

Diagnosis, — ^The  first  point  of  observance 
in  cases  of  suspected  tooth  impaction  is  an 
examination  of  the  dental  arches.  Are  all  of 
the  permanent  teeth  in  position  ?     Given  the        '^         -  -^ 

absence  of,  for  example,  a  lower  third  molar     .    ^'f^^  Photograph,  show 

'  r      '  ing    the     malposed     cuspid 

from    the    dental    arch,  with    a    history    of    no       entirely    embedded    in    the 

I  .  ,    .  .  bone  and  pressing  upon  the 

eruption,  and  a  persistent  neuralgia,  particu-  central. 
larly  if  occasionally  accompanied  by  or  alter- 
nated with  heavy  rheumatic  or  what  are  known  as  bone  pains,  and 
finding  no  other  evident  cause  of  the  neuralgia,  an  impactetl  tooth 
would  be  naturally  diagnosticated  as  the  source  of  the  disturbar.«e. 
Impacted  teeth  which  lie  horizontally,  or  nearly  so,  along  the  palatal 
vault  frequently  cause  a  swelling.  This,  taken  in  conjunction  with 
the  absence  of  a  tooth  from  the  dental  arch,  points  to  a  diagnosis  of 
impaction. 

In  very  many  cases  of  impaction  diagnosis  has  been  a  mere  accident, 
discovery  being  made  in  the  course  of  an  exploratory  surgical  oper- 
ation. ]\Iodern  science  solves  with  the  x-rays  the  difficulties  attentlant 
upon  the  diagnosis  of  impacted  teeth.  B.  H.  Catching*  was  the  first 
to  practically  apply  this  diagnostic  test  in  this  connection.  The  left 
upper  central  incisor  of  a  female,  aged  nineteen  years,  became 
loosened,  and  an  exploration  through  its  pulp  chamber  revealed  a 
hard  body  occupying  a  position  part  way  up  the  root,  which  had 
undergone  resorption  to  that  point.  The  cuspid  of  the  left  side  was 
absent  from  the  arch.     A  skiagraph  of  the  parts  (Fig.  237)  revealed 

>  Catching's  Compend,  1896. 


266     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

the  missing  cuspid,  whose  crown  had  impinged  upon  and  caused 
resorption  of  the  root  of  the  central  incisor. 

Impacted  teeth  may  become  uncovered  at  some  aspect  late  in  life 
and  the  condition  be  discovered  incidentally.  Cases  are  recorded 
where  the  pressure  of  a  plate  has  caused  the  resorption  of  tissues 
overlying  an  impacted  tooth,  thus  revealing  its  presence.  Fig.  238 
illustrates  a  case  where  the  presence  of  an  impacted  cuspid  was 
revealed  at  the  age  of  seventy  years,  through  resorption  of  the  alveolar 
bone  and  the  gum  tissue  covering  the  tooth. 

As  the  smooth  feel  of  enamel  is  a  diagnostic  feature  when  instru- 
mental examination  is  made,  it  is  to  be  remembered  that  the  enamel 
and  dentine  of  an  impacted  tooth  may  undergo  a  true  resorption 
with  the  characteristic  Howship's  lacuna?.  When  partly  exposed  to 
the  oral  fluid  caries  may  occur.  Both  these  conditions  produce  rough 
surfaces,  but  enamel  may  usually  be  felt  at  some  point. 

Fig.  238 


Impacted  cuspid  revealed  by  resorption  of  the  overlying  tissues      (Burchard.) 


Treatment. — The  treatment  of  cases  of  impaction  is  the  removal 
of  the  offending  tooth.  Whether  or  not  this  comes  within  the  province 
of  the  dental  operator  depends  upon  the  position  of  the  tooth,  and, 
incidentally,  upon  the  usual  range  of  practice  of  that  particular  prac- 
titioner. When  the  tooth  is  embedded  deeply  in  the  substance  of  the 
jaw,  access  to  it  involves  the  etherization  of  the  patient  and  the  removal 
of  the  bone  which  obstructs  the  path  of  extraction;  this  may  be  an 
operation  of  some  magnitude,  and  is  usually  done  by  a  special  sur- 
gical practitioner.  When,  however,  it  is  evident  that  the  obstructions 
to  the  removal  of  the  tooth  consist  of  the  soft  tissues  and  but  a  lamina 
of  bone,  the  operation  for  removal  is  clearly  within  the  province  of 
the  dental  operator.     For  example,   the  presence  of  an   impacted 


MACROSCOPIC  MALFORMATIONS  2G7 

cuspid  is  determined  lying  horizontally  along  the  lateral  aspect  of  the 
roof  of  the  mouth.  The  parts  may  be  injected  with  a  cocaine  or 
eucaine  solution,  and  a  curved  cut  made  with  a  sharp  bistoury  through 
the  soft  tissues  from  the  outside  of  the  swelling  to  the  bone.  The 
flap  thus  outlined  is  raised  from  the  bone,  the  flap  including  the  peri- 
osteum. A  large,  sharp  bur  is  then  employed  to  remove  the  covering 
bone.  When  the  tooth  is  freely  exposed  it  may  be  dislodged  with 
forceps  or  elevator.  The  parts  are  then  washed  with  a  hydrogen- 
dioxide  solution,  dried,  the  flap  pressed  back  into  place,  and  steresoP 
painted  over  the  parts. 

•  Dental  Cosmos,  1895: 

I^. — Purified  gum  lac g;^ 

Purified  gxun  benzoin g  1 

Balsam  of  tolu *  i 

Oil  of  cinnamon  (Chinese) *  i 

Acid,  carbolic «;{: 

Saccharin .  ^  i 

^'«=°'^o' Oij— M.  (Berlioz.) 


SECTION  III. 

AFFECTIONS  OF  THE  ENAMEL  AND  DENTINE. 


CHAPTER  IX. 

ABRASION,  EROSION,  AND  STAINS. 

MECHANICAL  INJURY  OF  THE  TEETH. 

Formed  by  the  ameloblasts,  later  changed  into  Nasmyth's 
membrane,  and  borne  upward  with  the  crown  during  the  process  of 
eruption,  enamel  has  no  posteruptive  source  of  nutritive  supply 
from  without. 

Its  only  conjectural  source  of  nutrition  is,  therefore,  from  the  pulp 
via  the  dentinal  tubuli.  Of  this  there  is  no  positive  proof  beyond 
that  offered  by  Caush.  (Sec  p.  164.)  Teeth  do  change  in  color  with 
advancing  age,  but  this  is  probably  due  to  changes  in  the  color  of  the 
dentine  transmitted  through  enamel,  which  is  normally  almost  or 
even  quite  transparent.  Such  a  transparency  may  be  seen  at  the 
incisal  edges  of  thin  incisors  before  these  edges  are  worn  down. 
Another  proof  of  transmission  of  color  through  enamel  is  seen  in 
caries;  a  bluish  black  or  white  appearance  is  caused  by  the  decayed 
mass  or  decalcified  inner  surface  of  the  enamel. 

Again,  amalgam  or  gold,  oxyphosphate  or  oxychloride,  reflects  its 
color  through  enamel,  and,  in  excavating,  the  shadow  of  the  excavator 
may  be  seen  through  thin  walls.  Enamel  may  be  stained  or  whitened 
by  decalcification  due  to  causes  acting  externally.  Extreme  polishing 
may  also  cause  a  new  character  of  light  reflection  simulating  a  change 
in  color.  Talbot  claims  a  change  in  color  of  teeth  during  prolonged 
illness,  such  as  pneumonia,  typhoid  fever,  syphilis,  tuberculosis,  and 
in  pregnancy.* 

After  implantation  a  tooth  may  somewhat  change  its  color,  but  this 

>  Dental  Cosmos,  1905,  p.  49. 


270  ABRASION,  EROSION,  AND  STAINS 

evidently  cannot  be  due  to  nutrition  from  the  pulp,  as  this  organ 
will  have  been  removed  before  implantation. 

It  is  generally  regarded  as  a  fact  that  while  enamel  may  suffer 
mechanical  and  chemical  injury,  it  undergoes  no  constructive  changes 
or  retrograde  metamorphosis.  There  is,  however,  a  possibility  that 
a  molecular  change  may  occur  as  a  result  of  time,  environment,  or 
impact  of  mastication. 

The  dentine  and  cementum  contain  about  28  and  30  per  cent, 
of  organic  matter,  respectively,  and  stain  deeply  and  permanently 
with  great  readiness. 

Possessed  of  living  cells,  they  also  undergo  changes  in  their  structure 
under  the  influence  of  various  stimuli,  their  substance  being  added 
to  or  reduced  according  to  circumstances.  They  are  also  acted  upon 
by  mechanical  and  chemical  agencies,  if  exposed  to  their  influence. 


ABRASION. 

Abrasion  is  the  mechanical  wearing  away  of  tooth  substance. 

Occurrence. — It  occurs  most  commonly  upon  the  occlusal  surfaces 
of  teeth,  but  is  also  found  upon  the  approximal  and  labial  surfaces, 
the  labial  cervix,  and  more  rarely  upon  the  lingual  surfaces.  It  is 
also  seen  in  the  temporary  denture,  especially  in  the  molars,  and  is 
found  in  animals  (Figs.  249  and  250). 

Appearance. — Purely  abraded  surfaces  present  a  smooth,  flat  or 
concaved,  highly  polished  appearance.  The  surface  may  become 
stained  or  otherwise  altered  in  color,  or  subsequent  caries  may  remove 
its  smooth  surface. 

Occlusal  Abrasion. — Occlusal  wear  is  very  common,  and  occurs 
largely  with  men  who  chew  tobacco;  the  contained  silex,  being  gritty, 
acts  as  an  abrasive.  Such  wear,  due  to  the  use  of  hard  food  or  gritty 
substances,  is  seen  in  skulls  of  aboriginal  man.  Ottofy  describes  a 
peculiar  form  of  wasting  due  to  chewing  betel  nut  mixed  with  bay 
leaves  and  slacked  lime.  No  doubt  a  silicious  element  is  introduced. 
Some  degree  of  occlusal  wear  is  accepted  as  normal  to  all  teeth,  the 
act  of  mastication  producing  marks  or  facets  at  the  point  of  articu- 
lation of  antagonizing  teeth.  A  tip-to-tip  variety  of  occlusion  permits 
free  lateral  movement  of  the  lower  jaw  and  an  herbivorous  type  of 
articulation  causing  aljrasion.  It  is  also  frequent  in  those  cases  pre- 
senting the  first  degree  of  prognathism.     In  some  of  these  cases  the 


ABRASION  271 

labial  surfaces  of  the  upper  incisors  and  cuspids  and  the  linguo-incisal 
margins  of  the  lower  incisors  are  worn.  A  single  overlapped  lower 
tooth  may  abrade  an  upper  tooth  in  this  manner. 

The  gritting  of  teeth  is  also  a  cause.  This  gritting,  termed  "bruxo- 
mania,"  may  occur  only  at  night  or  for  a  few  minutes  each  day;  again 
it  may  appear  for  entire  days,  weeks,  and  months,  not  ceasing  even 
during  sleep.  In  such  cases  the  teeth  are  worn  down  flat.  Maria 
and  Pietkiewicz*  noted  12  cases  of  central  nervous  lesions,  mostly 
dementia,  developing  bruxomania;  also  it  has  been  noted  in  cases 
of  epilepsy  and  chorea. 

A  clay  pipe  stem  may  wear  a  hole  of  its  own  diameter  in  the  incisal 
edges  of  anterior  teeth;  other  stems  wear  less.  Upholsterers  and 
seamstresses  have  peculiar  abrasions. 

The  undue  loss  of  posterior  occlusion  and  consequent  overuse  of 
the  anterior  teeth  cause  their  abrasion  after  the  manner  shown  in 

Fig.  239 


Abrasion  of  anterior  teeth,  with  loss  of  posterior  occhision.     (W.  A.  Capon.) 

Fig  230.  A  marked  overbite,  produced  in  any  manner,  may  cause 
lingual  abrasion  of  upper  anterior  teeth. 

Where  the  abrasion  occurs  in  a  fairly  regular  manner,  four  degrees 
of  abrasion  are  classified  (Figs.  240  and  241) :  (1)  Abrasion  removing 
the  cusps;  (2)  abrasion  renioving  the  occlu.sal  third  of  the  crown; 
(3)  abrasion  removing  the  middle  third  of  the  crown;  (4)  abrasion 
extending  to  the  gum  line  or  beyond  (Broca). 

When  there  is  a  marked  overbite  occulsion,  with  a  consequent  lessen- 
ing of  the  lateral  movement  of  the  mandible,  the  teeth  do  not  acquire 
flattened  contact  surfaces,  but  their  cusps  increase  in  sharpness 
and  pointedness.  This  at  times  becomes  exaggerated  and  produces 
an  interlocking  of  cusps  or  rather  worn  surfaces  which  have  very 
sharp  edges. 

In  the  first  degree  of  abrasion  the  dentine  is  often  hollowed  out  in 

>  Dental  Cosmos,  1907,  p.  525. 


272 


ABRASION,  EROSION,  AND  STAINS 


advance  of  the  enamel  of  the  cusps,  forming  concave  places  in  which 
berry  seeds  lodge  and  cause  annoyance.  These  spots  are  at  times 
hypersensitive. 

Labial  and  Approximal  Abrasions. — Some  forms  of  abrasion  have 
been  attributed  to  too  vigorous  use  of  tooth-brushes,  particularly 

Fig.  240 


The  first  and  second  degrees  of  abrasion.     Specimens  from  museum  of  Phila- 
delphia Dental  College. 

Fig.  241 


Tlie  third  and  fourth  degrees  of  abrasion.      Secondary  dentine  plainly  visible. 
.Specimens  from  museum  of  Philadelphia  Dental  College. 

when  gritty  powders  are  employed.  There  is  no  doubt  that  mechanical 
abrasion  about  the  necks  of  teeth  is  produced  in  this  manner,  the 
gum  line  receding  beyond  the  enamel  border,  exposing  the  cementum; 


ABRASION  273 

but  a  careful  examination  will  reveal  the  cementum  and  next  the 
underlying  dentine  to  be  affected;  the  enamel,  when  abraded,  shows 
first  as  a  facet  then  as  a  spot  of  bare  dentine  with  thin  edges  of  enamel 
around  it  (see  the  left  lateral  in  Fig.  257),  and  later  the  area  may  be 
grooved.  As  a  rule,  however,  the  effect  shown  in  Fig.  256,  lower 
jaw,  is  the  more  common.  These  tooth-l)rush  abrasions  are  quite 
characteristic.  In  well-kept  dentures  the  gums  are  seen  to  have 
receded  from  their  normal  line,  but  may  exhil)it  little  evidences  of 
turgescence;  the  roots  of  the  teeth,  upper  and  lower,  are  exposed  to 
a  greater  or  less  extent  along  their  labial  and  buccal,  but  not 
usually  along  their  lingual  aspects;  and  they  are  excavated  to  vari- 
able depths,  uj)()n  the  l)icuspids  and  first  molars  more  than  upon  the 
other  teeth,  as  here  the  greatest  force  of  brushing  is  received.     The 

Fig.  242 


Abnisioii  due  to  ein|)loyment  for  twenty  years  of  a  Kritty  Ijiglish  tooth  paste. 
At  7,  gold  crown  abraded.      (Miller.) 

depressions  have  a  normal  dentine  color,  sometimes  deepened  in  the 
mouths  of  non-smokers,  and  which  in  smokers  may  be  periodically 
blackened  by  deposits  of  carbon.  If  caries  supervene,  the  abraded 
areas  lose  their  normal  color,  and  may  l)e  readily  indented  by  sharp 
instruments,  which  they  resist  before  the  advent  of  caries.  The 
bicuspids  and  molars,  particularly,  may  be  grooved  in  such  maimer 
as  to  require  restoration  by  fillings. 

Miller'  investigated  thissul^ject  very  carefully,  and  found  that  the 
grit  in  many  forms  of  tooth  powder  vigorously  used  was  fjuite  compe- 
tent to  wear  away  tooth  structure,  gold,  and  other  lillings  ( Figs.  242  to 
245).  Figs.  244  and  247  show  a  lingual  wasting  resembling  graphic 
erosion.  In  both  cases  abrasion  is  proved  by  the  wasting  of  metal, 
which  acids  could  hardly  accomplish.     Miller  ex])criinentally  proved 

'  Dental  Cosmos,  1907. 

18 


274 


ABRASION,  EROSION,  AND  STAINS 
Fig.  24a 


Photomicrograph  of  sediment  obtained  by  wasliing  tooth  paste,  which  caused  the 
abrasion  shown  in  Fig.  242.      (Miller.) 


Fig.  244 


A     B 


Abrasion  of  lingual  .surface  by  assiduous  brushing  with  tooth  powder.      At 
D  and  E,  amalgam  worn  down.      (Miller.) 


ABRASION 


275 


abrasion  competent  to  produce  the  grooves  known  as  "wedge-shaped 
defect"  (Fig.  245). 

Fio.  245 


Artificial  abrasion  produced  by  brushing  witli  a  much-used  English  tooth  paste  with  motor 
brush  for  eighteen  hours.      Remains  of  gold  filling  in  first  bicuspid.      (Miller.) 

Calcuhi.s  may  he  worn  in  Hke  manner,  cither  l)y  the  bru.sh  or  by 
the  festoon  of  a  phite  (Fig.  248j. 

Fio.  240 


Gradual  wear  of  both  tooth  substance  and  filling  material  notwithstanding 
the  open  bite.      (Miller.) 

Miller  found  that  among  chnic  patients  who  never  used  a  tooth- 
brush the  labial  abrasion  was  wanting,  and  he  has  observed  that  a 


276  ABRASIOX,  EROSION,  AXD  STAIXS 

cessation  of  wear  followed  the  abandonment  of  the  use  of  gritty  powder 
and  the  adoption  of  a  soft  brush  and  mild  powder,  which  is  the  evi- 
dent indication  in  such  a  case. 

A  clasp  may  abrade  a  tooth,  and,  if  food  debris  be  retained  on  its 
inner  side,  caries  may  follow  in  the  abraded  area.  The  purely  abraded 
surface  will  be  polished.  Slight  approximal  abrasion  may  be  normal 
as  a  facet,  due  to  the  rubbing  of  one  tooth  upon  another  at  the  contact 
point.  A  marked  example  of  this  was  seen  in  the  mandible  jaw  of  a 
skull  of  a  jNIaori. 

The  third  lower  molars  are  locked  beneath  the  distal  surface  of 
the  crowns  of  the  second  molars.  Some  form  of  bone  loss  occurred, 
producing  looseness  of  the  third  molars.  The  individual  motion  of 
the  teeth  produced  a  deep  abrasion  of  the  enamel  of  the  second  molars 
upon  the  distal  surface  and  an  occlusoproximal  abrasion  of  the  third 
molars. 

Grit  in  powder  may  easily  be  detected  by  taking  a  small  portion 
between  the  incisor  teeth,  or  may  be  found  by  elutriating  the  powder; 
i.  e.,  place  in  water,  stir,  let  settle  for  a  few  seconds,  pour  off  the 
supernatant  fluid,  and  examine  the  sediment  as  above  or  microscop- 
ically (Fig.  243). 

^Miller  found  from  experiments,  as  to  the  effects  of  various  acids 
acting  for  a  time  and  followed  by  brushing  with  abrasives,  that  it 
depends  very  materially  upon  the  nature  of  the  acid.  Those  acids 
which  rapidly  decalcify  (soften)  the  dentine,  of  which  we  may  take 
hydrochloric  and  lactic  as  types,  most  readily  retard  the  wearing 
away  by  friction  (unless  the  friction  be  so  great  as  to  wear  in  spite 
of  the  decalcification).  \Miile  those  which  act  slowly  on  the  dentine 
(oxalic,  tartaric,  etc.),  as  well  as  those  which  have  a  macerating 
effect  on  decalcified  dentine,  may  be  wanting  in  this  influence.  He 
concluded  that  wear  could  not  be  produced  by  acid  alone,  but 
that  any  acid  or  acid  salt  which  possesses  the  power  of  extracting 
the  calcium  salts  from  enamel,  or  of  breaking  up  the  connection 
between  the  enamel  prisms,  may  accelerate  the  process  of  wasting, 
provided  the  necessary  mechanical  factor  works  together  with  it. 
Miller  found  food  to  be  a  negligible  quantity  as  to  wear  upon  labial 
surfaces. 

The  editor  has  a  patient  presenting  the  general  characteristics 
of  Fig.  258,  who  has  been  a  brush  enthusiast,  and  was  taught  in  early 
life  to  use  a  toilet  soap  containing  fine  pumice  (Bazin's  poncine 
soap) . 


ABRASION 


Zu 


Extensive  approximal  abrasion  may  be  due  to  extrusive  elongation 
of  a  tooth  in  one  or  both  jaws,  causing  a  tooth  to  oechide  with  its 
antagonist  with  a  glancing  motion. 

In  this  manner  specimens  are  produced  abraded  from  the  occluso- 
approximal  angle  to  nearly  the  apex  of  the  root. 

The  festoon  of  a  metal  plate  may  rapidly  cause  abrasion  of  the 
lingual  cervix  of  a  tooth.  The  condition  is,  however,  rare,  caries 
being  more  common.  In  the  editor's  practice  a  case  was  seen  in 
which  several  teeth  were  so  affected  in  a  few  months  by  an  ill-fitting 
metal  plate.  The  festoon  of  a  vulcanite  plate  has  also  produced 
such  an  abrasion. 

Abrasion  sometimes  follows  caries  when  the  latter  has  l)ecome 
freely  exposed  to  attrition.  The  softened  surface  wears  away  and 
the  part  assumes  a  polished  appearance,  but  is  discolored  as  the  result 
of  the  stain  due  to  the  caries.      (There  is  also  eburnation,  which  see.) 

It  is  probable  that  a  hyperacid  condition  of  the  saliva  in  connection 
with  mechanical  forces  may  be  a  cause  of  rapid  abrasion.  (See 
Erosion.) 

Effects  of  Abrasion. — These  are  external  and  internal,  and  most 
marked  in  the  occlusal  variety.  The  crown  wears  down  until  at  times 
the  gum  is  reachetl.  In  the  process  sharp  edges  of  enamel  are  formed. 
These  splinter  off,  leaving  rough  edges,  or  the  enamel  may  fracture 
or  split  longitudinally,  following  the  axis  of  the  crown.  Supported  by 
dentine  it  does  not  further  break  away  (Fig.  265). 

Sharp  enamel  edges  may  irritate  the  tongue,  producing  ulcers  of  a 
sometimes  chronic  type  which  acquire  indurated  edges  and  simulate 
syphilitic  sores  or  epithelioma.  The  causal  relationship  between  sharp 
edges  of  the  teeth  and  lingual  epithelioma  appears  to  be  quite  clear 
in  some  cases. 

Sores  which  have  given  evidence  of  malignancy  and  been  diagnos- 
ticated as  malignant  growths,  have  been  cured  by  rounding  and 
polishing  sharp  and  irritating  enamel  edges  of  teeth. 

The  continued  stimulation  of  the  ends  of  the  dentinal  fibrilla\  which 
are  exposed  in  abrasion,  causes  them  either  to  become  hypersensitive 
or  stimulates  them  to  formative  activity.  Tubule  material  is  built 
upon  the  inner  walls  of  the  tubule,  obliterating  their  lumen.  This 
is  the  so-called  tubular  consolidation  or  calcification  (eburnation). 
Accompanying  this,  secondary  dentine  is  often  formed.  As  a  result, 
most  commonly  the  pulp  chamber  of  the  crown  is  filled  up  with  sec- 
ondary dentine  as  the  abrasion  proceeds,  and  the  crown  may  often 


278 


ABRASION,  EROSION,  AND  STAINS 


be  worn  off  until  the  cervix  is  reached  while  the  pulp  remains  vital 
and  covered  (Fig.  241).     In  some  cases  the  abrasion  closely  approaches 


Fig.  247 


Fig.  248 


o,  abrasion  of  lingual  surfaces;   b,  of  amalgam  filling 
produced  by  a  plate.      (Miller.) 


Abrasion  of  calculus. 
(Miller.) 


Fig.  249 


Fig.  250 


Abrasion  of  lower  incisors  of  a  horse  pro- 
duced by  "cnbbing."    (Miller,  after  Kitt.) 


Defects,  resembling  wasting  in  the  teeth  of 
a  sea  lion.      (Miller,  after  Murie.) 


ABRASION  279 

the  pulp,  which  has  failed  to  protect  itself,  probably  because  of 
atrophy  of  odontoblasts  (Fig.  241),  and  the  phenomena  of  hyperemia, 
or  even  exposure,  and  its  residts  occur. 

The  causes  and  phenomena  of  abrasion  of  the  temporary  teeth  are 
practically  the  same  as  in  the  case  of  adults,  except,  perhaps,  that 
children  are  more  subject  to  the  action  of  rectal  parasites,  as  ascaris 
lumbricoides,  tenia,  etc.,  or  suffer  from  irritable  bladder  due  to  hyper- 
acidity of  the  urine.  These  conditions  commonly  produce  a  reflex 
stimulation  of  the  muscles  of  mastication,  resulting  in  nocturnal 
gritting  of  the  teeth. 

Treatment  of  Abrasion. — In  the  cases  of  cupped  occlusal  dentine, 
hard  fillings  of  gold  or,  preferably,  platinum  gold  are  advisable. 

If  nearly  all  teeth  are  present  and  the  abrasion  slight,  bridge-work 
may  be  used  to  restore  the  full  occlusion  without  attempt  at  restoration 
of  the  worn  surfaces. 

Flo.  251 


Same  case  as  Fig.  239.     Kite  opened  by  bridge-work,  posteriorly.      Anterior  teeth 
restored  by  means  of  Land  jacket  crowns.     (W.  A.  Capon.) 

If  the  abrasion  of  the  upper  anterior  teeth  be  deep,  the  bite  may 
be  raised  by  appropriate  posterior  crowns  or  bridges,  and  solid 
platinum-gold  fillings  may  be  built  upon  the  anterior  teeth,  either  the 
uppers  alone  or  upon  i)oth  the  upper  and  lower  teeth.  Anchorage 
may  be  obtained  in  the  dentine,  or  screws  may  be  planted  in  the  dentine 
between  the  enamel  and  pulp  and  the  fillings  be  built  about  them. 
Instead  of  malleted  fillings,  tips  of  the  gold-inlay  type  may  be  made 
(Figs.  252  and  253).     Casting  the  inlay  is  a  simpler  method. 

For  those  cases  in  the  second  degree,  as  a  means  of  limiting  the 
abrasion,  Dr.  J.  C.  Curry  has  introduced  small  cones  of  unaimealed 
iridioplatinimi  truncated  at  both  ends,  which  are  to  be  cemented 
into  holes  drilled  into  the  occlusal  faces  of  the  molars  and  bicuspids 
with  an  inlay  drill  of  exactly  corresponding  size  mounted  in  the 
right-angle  hand  piece.     As  many  are  put  in  as  the  safety  of  the  pulp 


2S0 


ABRASION,  EROSION,  AND  STAINS 


and  the  enamel  will  permit.  They  act  upon  the  same  principle  as 
steel  nails  in  a  shoe  heel. 

In  other  cases,  after  securing  a  proper  opening  of  the  bite  and 
posterior  occlusion  with  crowns  or  bridges,  single  porcelain-faced 
gold  or  platinum  crowns  may  be  made  to  cover  each  of  the  anterior 
teeth.  For  this  purpose  the  crown  is  appropriately  reduced  to  con- 
venient form,  but  the  pulps  need  not  be  destroyed.  Fig.  254  repre- 
sents the  method  outlined  by  Evans.^  There  can  be  no  objection  to 
pulp  removal  in  any  of  these  cases,  if  for  any  reason  a  dowelled  crown 
seem  preferable. 

Land  jacket  crowns,  consisting  of  a  wedge-shaped  platinum  jacket 
with  a  porcelain  facing  atta-ched  by  means  of  one  of  the  numerous 


Fig.  252 


Fig.  253 


Fig.  254 


Gold  tip  for  abraded 
teetli  with  living  pulp.s. 
(Evans.) 


Gold  tip  for  abraded 
teeth  with  pulp.s  removed. 
(Evans.) 


Porcelain-faced  crown.s 
for  teeth  with  living 
pulps.     (Evans.) 


inlay  bodies,  may  be  used  instead  of  the  Evans  crown.  In  some  cases 
other  forms  of  crowns  may  be  indicated  (Fig.  251). 

There  present  at  times  cases  of  abrasion  in  which,  aside  from  the 
wear,  pyorrhetic  conditions  may  be  present,  or  where  bridges  cannot 
be  properly  inserted. 

If  this  pertain  to  the  upper  jaw  only,  the  lower  denture  may  be 
restored  to  usefulness,  the  upper  teeth  extracted,  and  a  full  upper 
denture  in.serted;  this  permits  the  adjustment  of  the  bite  to  any  desired 
level.  If  the  condition  be  transferred  to  the  lower  jaw  and  the  anterior 
teeth  be  in  good  condition,  a  piece  of  tlie  (iriswold  type  may  be  fixed 
upon  cuspid  or  bicuspid  crowns. 

It  is  to  be  remembered  that  in  any  case  of  o})ening  of  the  bite  the 
occlusion  is  to  be  restored  throiigliont. 

'i'he  bite  must  not  be  raised  by  nieuiis  of  })artial  plates  which  strike 


'  Crown  and  Biidge  Work. 


RESORPTION  OF  ENAMEL  281 

before  the  natural  or  crowned  teeth,  as  they  tend  to  embed  themselves 
in  the  soft  tissues  and  create  inflammation. 

If  the  bite  be  only  slightly  raised  by  plates,  this  embedding  will 
cause  a  return  to  the  original  condition. 

In  case  of  hypersensitivity,  Robinson's  remedy,  silver  nitrate, 
nitric  acid,  or  the  electrocautery  may  l)e  efl'ective;  if  not,  the  areas 
should  be  excavated  and  filled,  or,  if  necessary,  the  pulp  should  be 
devitalized. 

If  the  abrasion  be  caused  by  tobacco,  its  use  should  be  stopped. 

A  difficult  class  of  cases  to  treat  is  found  in  those  highly  nervous 
individuals  who  grit  their  teeth  during  sleep.  It  is  prol)able  and 
reasonable  that  this  cause  alone  may  serve  to  explain  abrasions  trace- 
able to  no  other  source.  The  cure  of  such  cases  as  these  could  only 
be  possible  through  the  wearing  at  night  of  some  modified  form  of 
interdental  splint.  The  cases  naturally  indicate  the  medicinal  use  of 
a  bromide  before  retiring,  unless  the  causes  can  be  discovered  and 
removed. 

If  such  gritting  be  present  in  children,  the  evidences  of  irritable 
bladder,  due  to  hyperacidity  of  the  urine  or  of  rectal  parasites,  should 
be  sought  and  treated.  The  urine  may  be  rendered  alkaline  by  the 
use  of  potassium  salts  and  kept  so  by  restriction  to  a  largely  vegetable 
diet.  Belladonna  may  be  used  to  reduce  vesical  irritability.  Rectal 
parasites  may  be  removed  by  the  use  of  vermifuges,  or,  occasionally, 
by  rectal  injections. 

RESORPTION  OF  ENAMEL. 

Definition. — Resorption  of  enamel  is  the  removal  of  enamel  substance 
by  soft  tissue  containing  osteoclasts. 

Fig.  2.'i5 


Impacted  cuspid  with  resorptidii  of  eiumiol  and  a  liciiiatoKeiiic  calculus.      (Miller.') 

Occurrence. — It  occurs  externally  only  in  impacted  teeth  surrounded, 
at  least  in  part,  by  irritated  tissue,  aiul  internally  very  rarely  after 
resorption  of  dentine  by  the  pulp^  (Fig.  255). 

'  Hopewell-Sniitli,  Histology  and  Patliohistology  of  the  Teeth. 


282  ABRASION,  EROSION,  AND  STAINS 

Such  tissue  is  found  in  dermoid  cysts,  and  causes  the  resorption 
of  teeth.     (See  p.  63.) 

Pathology  and  Morbid  Anatomy.— Osteoclasts  approximate  the 
enamel  as  they  do  cementum,  decalcify  and  resorb  it.  The  dentine 
is  next  attacked.  There  result  irregular  excavations  (Howship's 
lacunae)  and  white  or  discolored  areas  of  evident  slight  decalcification 
of  the  enamel.  A  deposition  of  bone  into  the  area  may  occur.^  The 
process  is  probably  the  result  of  a  non-septic  inflammation,  as  in  the 
case  of  root  resorption.     (See  Interstitial  Gingivitis.) 

The  enamel  may  be  resorbed  from  its  internal  surface  after  the 
resorption  of  dentine  by  the  pulp  (see  Chapter  XVII),  and,  as  shown 
by  Woods,  may  be  filled  in  with  adventitious  material  of  a  structure 
resembling  cementum. 

Treatment. — Should  the  disease  by  chance  occur  upon  a  tooth  which 
later  has  been  drawn  into  place,  the  area  may  be  filled;  otherwise  it 
has  only  a  pathological  interest. 

EROSION. 

Definition. — Erosion  of  the  teeth  is  a  term  applied  to  the  chemical 
or  chemicomechanical  destruction  of  the  hard  tissues  of  the  teeth 
in  such  a  manner  that  broad,  shallow,  smooth  excavations  are  made 
in  the  enamel  and  dentine  in  situations  free  from  attrition  by  masti- 
cation. 

Figs.  256,  257,  and  258  illustrate  the  characteristic  appearance  of 
areas  until  recently  supposed  to  be  due  to  the  chemical  or  chemico- 
mechanical solution  which  has  been  termed  erosion. 

The  demonstrations  of  Miller  with  reference  to  abrasion  of  labial 
and  lingual  surfaces  of  teeth  by  means  of  the  tooth-brush  and  gritty 
powders,  and  the  abrasion  of  approximal  surfaces  into  grooves  in 
animals  by  the  drawing  of  gritty  grasses,  etc.,  through  or  along  the 
teeth,  or  the  gnawing  of  }>ones  by  carnivora,  etc.,  have  cast  a  heavy 
cloud  of  doubt  upon  the  chemical  etiology  of  what  have  been  usually 
considered  as  erosions  due  to  the  action  of  acid  sodium  phosphate 
excreted  by  the  mucous  glands  of  the  lips  or  cheek. 

The  appearance  ilhistrated  in  Fig.  256,  lower  jaw,  and  in  Figs. 
257  and  258  might  readily,  in  tlie  light  of  Miller's  demonstrations,  be 
regarded  as  abrasion  if  the  causes  (brush  and  abrasive  powders)  he 
suggests  be  found,  but  the  graphic  outhnes  shown  in  Fig.  256,  upper 

'  Hopewell-iSrnitli,  Histology  and  I'atliohistology  of  the  Teeth. 


EROSION 


283 


anterior  teeth,  seem  difficult  to  harmonize  with  the  abrasion  theory. 
The  cases  of  this  sort  are  rare  as  compared  with  the  others,  the 
editor  recalhng  but  two  having  the  pecuHar  undercut  mesial  and  distal 
erosion  borders.  The  spreading  of  brush  bristles,  as  the  brush  is 
brought  from  the  gum  down,  might  account  in  part   for  this,  but  in 


Fig.  256 


Fig.   257 


Case  described  as  erosion.      (Darliy.) 


Case  described  as  erosion.     (Darby.) 


one  of  the  cases  mentioned  there  was  also  an  undercut  at  the  incisal 
border,  which  woidd  render  the  theory  difficult  of  application. 

One  case  was  in  a  man  aged  forty-five  years,  a  German  Jew,  fond  of 
wines,  beer,  etc.,  at  meals;  the  other  a  middle-aged  maiden  lady  of 
nervous  temperament,  with  whitening  hair,  slightly  wrinkleil  skin,  and 


some  evidences  of  goutiness. 


Fig.  258 


ts 


A  case  of  ero.sion  (drawn  from  the  ca.st):    B,  silhouette  from  a  perpendicular  line  tlirouKli 
the  left  centrals,  upi)er  and  lower,  showing  the  lo.ss  of  substance.     (Black.) 

According  to  Miller,  acids  or  acid  salts,  which  can  extract  calcium 
salts,  may  accelerate  the  wasting  process  provided  the  necessary 
mechanical  factor  works  with  it  and  wears  off  the  decalcified  tissue 
before  it  becomes  leathery,  when  wear  is  retarded.  Kirk  burnt 
asbestos  cloth,  treated  it  with  hydrochloric  acid,  neutralized  this  with 
ammonia,  washed  it  with  distilled  water,  and  again  subjected  it  to 


284  ABRASION,  EROSION,  AND  STAINS 

high  muffle  heat.  This  absorbent,  inorganic  cloth  he  appHed  to  buc- 
cal glands  for  twenty  or  thirty  minutes  in  cases  of  erosion,  dissolved 
the  mucus  obtained  in  distilled  water,  dialyzed  the  salts  out,  and 
examined  the  evaporated  residue  under  the  microscope  and  by 
reagents.  He  found  acid  sodium  phosphate  to  be  the  decalcifying 
agent  in  what  he  called  graphic  (hydroglyphic)  erosions  (Figs.  256 
and  257). 

Head^  found  by  experiment  with  a  1  to  20,000  solution  of  acid  sodium 
phosphate  in  water,  acting  in  the  incubator  at  body  temperature,  that 
superficial  decalcification  of  enamel  occurred  after  fourteen  hours, 
and  when  polished  off  it  again  decalcified  in  eight  hours,  and  was 
quite  superficially  decalcified  in  two  days;  that  a  5  per  cent.,  2  per 
cent.,  1  per  cent.,  and  1  to  500  solution  acted  under  similar  condi- 
tions in  seventeen  hours,  and  points  out  that  a  solution  of  1  to  10,000 
and  1  to  20,000  acid  sodium  phosphate  in  alkaline  saliva  acted  after 
eight  and  five  days  only. 

Miller  found  the  slowly  acting  acids  to  not  produce  such  decalcifica- 
tion as  to  retard  the  abrasive  action  of  brushing  with  a  10  per  cent, 
pumice.  Given,  then,  a  decided  production  of  acid  sodium  phosphate 
by  the  buccal  glands  in  contact  with  the  labial  surfaces  of  teeth 
(Kirk)  for  eight  hours  (the  period  of  sleeping,  and  Head's  period  of 
one  experiment,  see  above),  it  is  quite  reasonable  to  suppose  that  an 
undetermined  percentage  of  acid  sodium  phosphate  dissolved  in  buccal 
mucus,  which  in  total  has  an  acid  reaction  to  litmus  (Truman,  Kirk, 
and  others),  is  competent  to  produce  a  superficial  decalcification, 
which  the  morning  brushing  will  remove.  This  repeated  for  months  or 
years  may  produce  the  effect  seen.  Brubaker,  in  1894,  immersed  a 
tooth  for  a  week  in  a  solution  of  acid  sodium  phosphate,  subjecting  it 
daily  to  tooth-})rush  friction,  and  at  the  end  of  that  time  spots  and 
grooves  resembling  erosion  made  their  appearance. 

According  to  Head  and  Kirk,  the  acid  phosphate  does  not  attack 
the  enamel  so  as  to  roughen  it,  but  leaves  it  translucently  smooth  and 
white,  and  this  mildness  of  the  action  of  the  acid  sodium  phosphate 
is  just  the  action  that  would  make  smooth  erosion  with  a  minimum 
of  abrasion.     (See  Miller's  experiments,  p.  276.) 

Head  points  out  "that  1  to  500  lactic  acid  in  water  will  decalcify 
enamel  in  thirty  minutes,  while  the  same  percentage  in  saliva  does  not 
do  so  in  fifte(>n  days,  l>iit  that  the  inhibitory  effect  of  saliva  is  over- 
come when  the  lactic  acid  has  a  strength  of  1  per  cent."     The  inhib- 

1  Dental  Cosmos,  1907. 


EROSION  285 

itory  effect,  therefore,  seems  to  lie  in  the  relative  relations  of  the  acid 
and  alkaline  elements,  though  Head  has  shown  that  a  mixture  of  1 
per  cent,  solution  of  acid  sodium  phosphate  with  a  1  per  cent,  solution 
of  tribasic  sodium  phosphate,  which  is  capable  of  turniiiij  blue  litmus 
red,  but  not  of  turuiuf^  red  litmus  blue,  placed  the  acid  under  control 
so  that  the  mixed  solution  did  not  corrode  the  tooth  placed  in  it,  which 
a  1  per  cent,  solution  of  acid  sodium  phosphate  in  water  would  do. 

Regarding  the  production  of  the  abnormal  exudate  from  the  labial 
glands,  Kirk  argues  that  in  diseases  of  suboxidation  (resulting  in 
hyperacid  conditions  such  as  gout  and  rheumatism)  the  blood  is 
loaded  with  carbonic  acid  as  a  result  of  faulty  metabolism.  In  the 
epithelium  of  the  kidneys  the  mass  action  of  thecarl)onic  acid  upon  the 
sodium  phosphate  of  the  blood  normally  produces  acid  sodium  phos- 
phate, which  is  eliminated  in  the  urine,  and  sodium  bicarbonate,  which 
is  returned  to  the  blood  and  maintains  its  alkalinity  (see  p.  87), 
according  to  the  following  reaction :  HNajPO^  +  HjCOg  =  HjNaPO^ 
+  HNaCOg.  If  the  amount  of  carbonic  acid  be  of  only  normal 
production,  this  action  will  result  in  only  a  normal  amount  of  acid 
sodium  phosphate  in  the  urine  and  perspiration,  but  if  in  excess  and 
not  cared  for  hy  the  lungs,  skin,  and  kidneys,  the  buccal  glands  may 
also  take  up  the  action  and  excrete  acid  sodium  phosphate  in  an 
identically  similar  manner.  The  acid  calcium  phosphate  is  also 
found  in  the  saliva  at  times,  and  can  be  formed  in  a  similar  way,  the 
calcium  phosj)hate  being  substituted  for  sodium  phosphate  as  the 
basic  salt. 

Kirk  states  that  in  the  saliva  of  arthritics  there  are  frequently  foun<l 
acid  salts,  such  as  acid  sodium  phosphate  and  acid  calcium  phos- 
phate. The  excessive  amount  of  cari)onic  acid  accounts  for  the 
excessive  loss  of  phosphate  in  the  kidneys  seen  in  arthritics,  as  the 
acid  sodium  phosphate  and  acid  calcium  phosphate  require  for 
their  production  the  basic  phosphates,  and  the  elimination  of  those 
continuously  produces  a  phosphaturia  until  depletion  of  phosphates 
occur,  when  their  amount  lessens  and  other  salts  appear.      (See  p.  87.) 

In  a  paper  published  in  19t)2,  Kirk'  describes  polariscopic  observa- 
tions made  upon  saliva  from  a  patient  afflicted  with  a  general  erosive 
wasting  of  the  t(>cth.  The  patient  had  had  attacks  of  inflammatory 
rheumatism,  and  sutt'ered  from  obstinate  constipation,  periodic 
attacks  of  migraine,  headaches,  and  neuralgia,  and  his  saliva 
was   most   acid   at   night.     The   saliva   was   dialyzed,    tlu>   dialysate 

'  Items  of  Interest. 


^^ 


286 


ABRASION,  EROSION,  AND  STAINS 


concentrated  and  found  to  contain  lactic  acid  salts,  calcium  lacto- 
phosphate,  calcium  lactate,  and  magnesium  lactophosphate  (Fig.  259). 
In  view  of  these  two  classes  of  cases,  Kirk  has  suggested  that  erosion 
cases  may  be  of  two  kinds:  (1)  A  general  erosion,  in  which  all  of 
the  surfaces  are  uniformly  involved,  and  in  which  lactic  acid  is 
the  solvent  agent;  and  (2)  cases  distinctly  due  to  an  exudate  from 
abnormal  buccal  glands  or  gland,  the  acidity  of  which  is  due  to  either 
acid  sodium  phosphate  or  acid  calcium  phosphate.  Talbot^  claims 
that  the  systemic  acidosis  produced  by  various  diseases  and  by  fruit- 
eating  in  excess  is  responsible  for  the  acidity  of  the  buccal  mucus 
and  saliva  and  for  pulp  and  gingival  degeneration  and   resorption 

Fig.  259 


A' 

Crystallization  of  salts  from  dialysate  of  saliva  from  erosion  case,  showing  two  typal  forms 
Large  crystal  is  calcium  lactate.     (Kirk.) 

through  a  process  of  artery  and  nerve-end  degeneration.  A  decrease 
in  the  nonnal  acidity  of  the  urine  (below  30)  indicates  renal  insuffi- 
ciency, and  the  difference  indicates  the  amount  retained  in  the  system. 
An  excessive  acidity  of  the  urine  indicates  excessively  imperfect 
oxidation.  This  expres.sion  of  the  cause  is  quite  compatible  with  the 
view  of  Kirk,  and  both  are  views  of  general  malnutrition.  (See  p. 
85,  etc.) 

The  disease  appears  to  affect  females  more  than  males;  appears 
usually  after  thirty  years  of  age,  and  often  some  history  of  goutiness, 
arthritis,  or  rheumatism  can  be  obtained.     Miller  denied  the  presence 


Dental  Cosmos,  December,  1907. 


EROSION 


287 


of  this  disease  in  the  gouty,  but  since  his  observation  the  editor 
has  had  two  patients  hold  up  gouty  fingers  when  questioned  as  to 
a  possible  gout  as  a  cause  of  the  erosions  present. 

Erosion  Due  to  Extraneous  Acids. — Miller^  describes  a  case 
reported  by  Davenport,"  of  Paris,  of  a  healthy  man  whose  teeth  were 
eroded  and  worn  away  by  acid  vapors  within  six  months  of  entering  a 
factory  devoted  to  the  manufacture  of  nitric  and  sulphuric  acids.  This 
effect  was  observed  upon  the  other  workmen  also,  and  also  in  workmen 
in  a  dynamite  factory  in  which  these  acids  are  used.  The  teeth  were 
first  set  on  edge.  Miller  suspended  a  tooth  in  a  flask  containing  equal 
parts  of  nitric  and  sulphuric  acid,  and  found  that  the  vapors  attacked 


Fig.  2G0 


Another  field  from  the  same  specimen  as  Fig.   259,  also  showing  two  typal   forms. 
Large  crystal  is  calcium  lactate.      (Kirk.) 

not  only  the  inorganic  but  the  organic  portion  as  well,  so  that  upon 
slight  rubbing  with  a  soft  tooth-bnisli  the  tissue  was  worn  away,  halving 
a  hard,  polished  surface.  Miller  states  that  the  vapor  is  nitrogen  per- 
oxide, N^O^.  Lemon  juice,  even  in  lemonade,  and  vinegar  will  produce 
this  effect  of  setting  on  edii^i^,  which  un(l()ubt(>(lly  is  due  to  the  chemical 
solution  of  a  small  {Portion  of  the  enamel,  j)r()hal)ly  the  iiiterj)ri.s- 
matic  cement  sul)stance,  leaving  the  enaniel  glol)iiles  a  triHe  higher, 
this  soon  being  worn  off  to  a  general  level  again. 

GuilfonP  mentions  a  case  of  erosion  caused  by  shaddock  (grape 
fruit)  eating.     Tomes  cites  cases  of  ero.sion  caused  In-  lemon  and  grape 


>  Dental  Cosmos,  1907. 
'  Lectures. 


2  Transactions  .\mericaii  Ucntal  .Association,  1881. 


288 


ABRASION,  EROSION,  AND  STAINS 


sucking.  The  pitting  of  grapes  has  produced  cases  of  peculiar  erosion 
of  the  labial  and  lingual  surfaces  and  incisal  edges  of  anterior  teeth. 
In  one  case  the  incisal  anchorage  of  an  approximal  gold  filling  was 
almost  worn  away  upon  the  tooth  most  used  to  pit  the  grape.  Un- 
questionably, other  fruit  juices  might  act  in  a  similar  manner  if  the  acid 
has  an  affinity  for  tooth  structure,  and  the  exposure  to  its  action  is 
sufficiently  lengthy  and  often  enough  repeated  to  produce  effects. 

The  Effects  of  Erosion. — Tubular  calcification  and  secondary  dentine 
are  produced  together  with  atrophic  changes  in  the  pulp,  due  to  second- 
ary dentine  formation.  Gold  and  amalgam  fillings  are  left  as  raised 
islands  by  the  wasting  of  the  tooth  around  them,  though  Miller  has 


Fig.  261 


'^'-j^^^^^^i 

■ 

mj^m 

^^H^l 

r^B 

^HH 

^B^^^-;^.-'^ 

i^,jifl 

1 

I^^hIP^jm/'' 

Crystallization  from  .solution  of  a  tooth  in   1  per  cent,  lactic  acid.     Large  crystal 
is  calcium  lactate.     (Kirk.) 

shown  that  associated  abrasions  may  cause  their  wear,  which  acids 
evidently  can  hardly  be  expected  to  <lo. 

Scratches  shown  as  lines  and  Baume's  clefts  are  explainable  upon 
the  theory  of  abrasion  by  brush  and  powders;  though  usually  trans- 
verse, there  are  sometimes  vertical  lines.  The  stimulation  of  the 
dentinal  fibrillar  by  acid  or  meclianical  stimuli  may  cause  great 
hypersensitivity;  as  a  rule,  however,  this  is  not  marked  (P^ig.  262). 

The  anterior  teeth  are  sometimes  shortened  so  that  their  occlusion 
is  lost.  Kirk's  lactic  acid  case  was  of  this  order.  The  carious  pro- 
cess may  become  implanted  upon  an  eroded  area,  or  at  some  part  of 
it,  usually  the  cervical  portion.    Whether  this  is  initiated  by  a  decalcify- 


EROSION 


289 


ing  process  due  to  the  acid  sodium  phosphate,  or  uncleanliness  due  to  a 
cessation  in  the  intensity  of  the  brushing,  is  not  so  clear  as  it  formerly 


Fig.  262 


F  C 


S  D 


EC 


Sagittal  action  of  liunian  incisor  prepared  by  Hopewell-Smith's  process,  and  stained  with 
hematoxylin:  E  C,  erosion  cavity,  on  surface  of  wliich  can  be  seen  Baume's  clefts;  P.  pulp 
tissue  undergoing  degenerative  changes;  F  O,  atrophic  odontoblasts;  S  D,  secondary  dentine. 
X  45.     (Hopewell-Smith.) 

seemed  when  it  was  thought  due  to  a  temporary  cessation  in  {)ro- 
duction  of  acid  sodium  phosphate,  which  was  regarded  as  immunizing 
the  part  to  caries. 
19 


290  ABRASION,  EROSION,  AND  STAINS 

Diagnosis. — The  presence  of  the  pecuKar  excavations,  the  hyper- 
sensitivity of  dentine  if  any,  and  the  acid  character  of  the  mucus 
from  the  foUicles,  as  shown  upon  test  with  htmus  paper  made  just 
after  rising,^  are  diagnostic  signs.  Kirk's  method  of  obtaining  the 
acid  may  be  used.  (See  p.  283.)  The  acid  reaction  is  not  marked 
during  the  day.  The  existence  of  erosion  has  become  a  vahiable  diag- 
nostic sign  for  the  general  practitioner  in  his  search  for  the  nature  of 
masked  maladies  from  which  patients  frequently  suffer.  Obscure 
gout  has  been  pointed  out  through  dental  indications  alone,  where  the 
practitioner  had  before  been  baffled  in  his  diagnosis. 

Treatment. — The  treatment  of  erosion  divides  itself  under  two  heads : 
prophylactic  and  restorative;  the  prophylactic  is  again  divided  into 
local  and  general  treatment.  The  problem  of  eradicating  the  cause 
of  the  disorder  lies  in  a  correction  of  the  morbid  glandular  secretion. 
It  is  evident  that  if  the  irritation  and  altered  secretion  of  these  glands 
be  due  to  some  systemic  cause,  a  disease  of  suboxidation,  notably  an 
affection  of  the  gout  order,  a  cure  of  the  local  disturbance  involves  the 
cure  of  the  underlying  systemic  cause.  Talbot^  reduces  the  acidity 
to  normal  with  sodium  bicarbonate  (10  to  30  grs.),  or  sodium  chloride 
(45  grs.),  after  meals;  or  sodium  phosphate  morning  and  evening. 
One-tenth  grain  of  calomel  is  given  each  two  hours  to  cleanse  the 
bowel  and  stimulate  the  liver.  Eight  to  ten  glasses  of  water  should 
be  taken  daily.  A  practically  antigout  diet  and  hygiene  are  sug- 
gested to  increase  oxidation  and  elimination.  Local  treatment  of  the 
gums  is  necessary.     (See  pages  97  and  98.) 

Next  in  importance  to  the  prevention  of  acid  formation  is  its  neutral- 
ization. This  implies  the  application  of  alkalies  or  the  use  of  alkaline 
mouth  washes.  The  greatest  production  of  acid  occurring  during  the 
night,  applications  of  adhesive  masses  of  alkaline  substances  are  made 
to  the  teeth  at  night.  The  principal  of  these  is  prepared  chalk,  calcium 
carbonate;  it  is  rubbed  over  the  labial  faces  of  the  teeth  and  between 
them,  before  retiring.  It  remains  in  sufficient  amount  to  neutralize 
any  acid  substances  coming  in  contact  with  it. 

Excellent  results,  as  to  the  checking  of  the  progress  of  the  decal- 
cifiation,  are  ol^tained  from  the  use  of  magnesium  hydrate  held  in 
suspension  in  water,  or  milk  of  magnesia.  Kirk  found  that  three  hours 
after  the  use  of  a  teaspoonful  of  the  milk  of  magnesia  the  saliva 
maintained  an  alkaline  reaction.  It  should  be  used  at  night  as  a 
wash,  after  cleansing  the  teeth,  the  residue  to  be  left  as  an  alkaline 

'  Truman.  '  Dental  Cosmos,  December,  1907. 


MECHANICAL  INJURY  OF  THE  TEETH  291 

coating  upon  the  teeth.  The  clmlk  and  milk  of  magnesia  may  be 
mixed  into  a  paste.  If  the  preparation  be  disagreeable,  a  few  drop.s 
of  essential  oil  may  be  added.  (See  p.  373.)  The  abrasive  factor 
and  its  possibilities  as  causes  of  apparent  erosions  suggest  the 
avoidance  of  any  strongly  abrasive  powders,  or,  perhaps,  a  confine- 
ment to  the  use  of  castile  soap  and  a  soft  brush. 

It  has  been  suggested  by  Ottolengui'  that  in  the  earlier  stages  an 
impression  and  plaster  model  of  the  teeth  be  made  for  comparison 
at  future  dates,  so  that  the  progress  of  the  erosion  may  be  noted. 

Restorative  Treatment. — If  the  eroded  areas  be  excavated  and 
filled,  the  erosion  may  proceed  about  the  edges  of  the  fillings.  It 
may,  however,  take  some  time  for  the  erosion  to  become  as  deep  as 
the  original  area. 

If  metal  be  used,  the  margins  must  be  extended  to  avoid  this  if 
possible.  INIetal  is  very  unsightly  in  the  locations  peculiar  to  erosion, 
so  that  porcelain  inlays,  which  the  locations  favor,  are  indicated.  In 
their  place  gutta-percha  or  oxyphosphate  fillings  may  be  used,  but 
must  be  constantly  kept  in  a  good  condition  of  surface  or  they  become 
unsightly. 

The  generally  distributed  erosions  are  only  amenable  to  the  prophy- 
lactic treatment  (except  by  crowning  when  teeth  are  largely  wasted 
away),  and  slight  erosions  are  best  treated  in  the  same  manner. 


MECHANICAL  INJURY  OF  THE  TEETH. 

The  enamel  is  a  material  much  more  brittle  and  inelastic  than  the 
dentine,  and,  therefore,  less  capable  of  resisting  a  parting  strain.  Under 
ordinary  circumstances,  however,  well-formed  enamel  distrilnited  over 
sound  dentine  resists  all  the  ordinary  forces  brought  to  bear  upon  it. 

Under  abnormal  conditions,  however,  enamel  a])pears  to  fracture 
readily  in  two  directions:  (1)  Along  the  line  of  the  interprismatic 
cement  substance  between  the  prisms  themselves,  and  (2)  along  the 
line  of  cement  substance  between  the  globides.  The  possibility  of 
reference  of  all  cases  into  one  or  other  class  indicates  that  the  cement 
substance  is  naturally  a  tissue  relatively  weak. 

Dentine  may  apparently  fracture  in  any  plane. 

Causes. — The  teeth  may  be  mechanically  injured  by  (1)  the  action 
of  abrasion,  which  mechanically  wears  away  the  teeth;  (2)  by  the 

>  Methods  of  Filling  Teeth. 


292  ABRASION,  EROSION,  AND  STAINS 

application  of  undue  force  during  mastication  or  by  the  improper 
use  of  cutting,  filling,  or  extracting  implements;  (3)  by  blows  of  some 
sort  delivered  either  directly  upon  the  teeth  or  through  forcible  closure 
of  the  jaws,  as  the  result  of  a  shock  or  blow  delivered  upon  the  rim 
of  the  jaw. 

Aside  from  blows  or  bites  of  sufficient  force  to  break  sound  teeth, 
it  is  rare  to  find  teeth  fractured  without  a  previously  acquired  weakness 
in  the  tooth  itself.     The  causes  of  weakness  are  several. 

During  the  course  of  abrasion  the  enamel  is  worn  to  a  sharp  edge, 
which  is  readily  fractured.  Oblique  splintering  occurs  in  the  line 
of  cement  substance  between  the  globules.  The  enamel  edges'  become 
ragged  and  further  fracture  is  imminent.  Thread  biting  produces  a 
similar  but  localized  condition  (Fig.  265). 

Caries  by  removing  the  natural  support  of  the  enamel  renders  this 
brittle  material  subject  to  fracture  in  ordinary  use.  The  removal  of 
dentine  from  both  the  mesial  and  distal  sides  of  a  crown  by  caries — 
e.  g.,a  bicuspid — renders  the  buccal  or  lingual  section  liable  to  fracture 
as  the  result  of  a  strain  delivered  between  the  cusps  and  tending  to 
wedge  them  apart.  This  accident  is  liable  to  occur  in  proportion  to 
the  lessening  of  the  healthy  dentine  between  the  cavities  or  beneath 
the  occlusal  fissure.  An  upper  incisor  so  decayed  would  naturally 
have  its  labial  section  fractured  away,  particularly  its  incisal  half. 

The  exposure  of  the  dentine  of  a  devitalized  tooth  to  the  saliva 
seems  to  weaken  it. 

WTiile  these  principles  are  correct,  it  is  surprising  to  what  extent 
enamel  undermined  by  caries  may  retain  its  integrity  if  properly 
supported  by  an  adhesive  oxyphosphate  of  zinc. 

The  packing  of  cohesive  gold  against  frail  enamel  walls  renders 
them  liable  to  direct  fracture,  or  if  packed  so  as  to  permit  leakage 
the  wall  is  further  weakened  by  lactic  acid  produced  upon  its  under 
surface.  Again,  the  improperly  prepared  cavity  margin  may  be 
comminuted. 

Gold  does  not  support  enamel  walls  so  well  as  oxyphosphate.  If 
built  over  comparatively  frail  walls  in  such  a  maimer  as  to  protect 
them  from  direct  impact,  they  stand  fairly  well. 

Amalgam  l^y  its  attendant  leakage  permits  gradual  weakening  of 
frail  enamel  walls.  The  use  of  a  cement  lining,  as  in  combination 
fillings,  is  distincdy  useful  both  as  a  support  and  prevention  of  leakage. 

Johnson^  explains  fracture  after  filling,  where  the  enamel  walls 

*  Principles  and  Practice  of  Filling  Teeth. 


MECHANICAL  INJURY  OF  THE  TEETH  293 

were  previously  undermined  but  not  fractured,  upon  the  theory  that 
previous  to  filling  the  pain  attendant  upon  mastication  brings  about 
a  temporary  disuse  of  the  diseased  tooth.  After  filling  comfort  ensues, 
the  patient  again  uses  the  tooth,  and  fracture  occurs. 

The  fractures  caused  by  blows  present  features  of  interest.  An 
actual  splitting  off  of  one  of  the  angular  portions  of  a  crown  may 
occur,  or  a  fracture  may  be  seen  resembling  one  sometimes  seen  in 
a  pane  of  glass  the  result  of  a  light  blow  from  a  stone. 

In  the  latter  case  the  cracks  radiate  from  a  central  crushed  spot, 
and  may  involve  only  the  enamel.  A  large  section  of  an  incisor  may 
be  fractured  away  and  include  the  labioincisal  third  and  all  the 
lingual  section  of  the  crown  and  a  small,  obliquely  fractured  portion 
of  the  root. 

Biting  upon  hard  objects  has  caused  the  fracture  of  sound  bicuspids 
and  molars,  the  line  extending  mesodistally  between  the  cusps,  and 
in  an  upper  tooth  through  the  crown  and  between  the  roots.  Thus, 
a  molar  or  first  bicuspid  may  be  divided  into  two  sections,  each 
supported  by  a  root  or  roots  (Fig.  264). 

Fracture  and  repair  of  enamel  after  eruption  is  not,  so  far  as  I  am 
aware,  known.     Cases  of  fracture  and  repair  of  dentine  have  occurred. 

A  case  of  such  repair  by  adventitious  (secondary )  dentine  has  been 
recorded  by  Tomes/  and  Fig.  266  illustrates  a  fracture  of  the  root 
well  below  the  gum  line.  The  root  is  girdled  by  the  line  of  fracture, 
but  the  dentine  has  been  repaired  and  the  attachment  is  firm.  The 
line  evidently  indicates  a  repair  from  the  pulp  side.  A  case  analogous 
to  healing  of  a  comminuted  fracture  of  a  central  has  been  reported. - 

Fig.  267  illustrates  a  peculiar  fracture  due  to  an  unknown  cause. 

In  a  case  reported  by  Val.  Macdonald,^  of  a  similar  fracture,  the 
pulp  maintained  its  vitality  for  two  years  and  until  the  tooth  was 
extracted. 

In  an  experimental  implantation  of  a  dried  tooth  filed  to  fit  the 
socket  of  a  previously  extracted  tooth  union  of  osseous  nature  took 
place,  and  a  slight  fracture  of  the  root  was  reunited  by  osseous 
deposition.^ 

Longitudinal  cracks  in  the  enamel  of  otherwise  fairly  sound  teeth 
occur,  the  line  running  from  the  labial  edge  of  the  gum  to  the  incisal 
edge  of  an  incisor  (Fig.  265),  or  from  the  fissure  of  a  bicuspid  along 

'  A  System  of  Dental  Surgery.     (See  Secoiulary  Dentine.) 

2  Watson,  Dental  Record,  May,  1906. 

•■'  Dental  Cosmos,  .January,  1908. 

*  Mendel  Josepli  and  Dessonville,  L'Odontologie.     (See  Cosmos,  1900,  p.  1000.) 


294 


ABRASION,  EROSION,  AND  STAINS 


the  enamel  to  the  summit  of  a  cusp,  or  from  the  cervical  margin  of 
an  approximal  cavity  to  the  gum  margin. 

These  lines  probably  indicate  that  force  has  been  applied  sufficient 
to  cause  a  parting  of  the  enamel  cap  without  loss  of  continuity  in  the 
more  elastic  dentine.    Dryness  from  mouth  breathing  may  be  a  possible 


Fig.  263 


Fig.  264 


Oblique  fracture. 


Fracture  involving  the  bifurcation  of  the  roots. 


cause  of  cracks,  and  the  contact  of  excessively  hot  or  cold  substances 
has  been  advanced  as  an  hypothesis.  In  some  cases  the  enamel 
cracks  may  be  very  numerous.  These  cracks  take  up  stains,  and  at 
times  in  the  preparation  of  cavities  cause  annoyance  by  centring 
the  chisel  and  perpetuating  a  defect  necessitating  the  removal  of 
much  tooth  tissue  or  the  risking  of  future  caries. 


Fig.  265 


Fig.  266 


Abrasion  associated  with  fracture  of 
the  enamel. 


Root  fracture  and  reattachment  by  adven- 
titious dentine.      (From  a  siJecimen.) 


Treatment. — The  treatment  of  fractures  involves  considerations 
purely  operative,  and  depends  upon  the  nature  of  the  case.  Rough- 
ened, abraded  enamel  margins  an;  Ix'st  rounded  v^ith  carborundum 
stones  or  coarse  sand-paper  disks,  and  should  l)e  polished.  Sometimes 
a  deep  serration  must  be  filled;  corners  are  to  be  neatly  rounded  or 


MECHANICAL  INJURY  OF  THE  TEETH 


295 


restored  to  contour  by  fillings  or  inlays,  or  at  times  the  entire  incisal  etige 
is  to  be  ground  away  and  the  tooth  drawn  down  and  retained  until  firm. 

In  case  of  an  uncompleted  tooth  root,  and  the  pulp  not  quite 
exposed,  a  ])ure  gold  all-metal  crown  is  to  be  adapted  with  or  without 
grinding,  according  to  the  future  rccjuirements,  and  the  root  completion 
awaited.  If  necessary,  the  capping  of  the  pulp  may  be  attempted  as 
well  for  the  same  purpose. 

After  root  formation  the  pulp  may  l)e  destroyed  if  desired.  If 
conservation  of  the  pulp  be  not  ])ossible,  the  pulp  may  be  prepared 
for  removal  by  pressure  anesthesia  or  cocaine  injection  and  the  root 
filled.     (See  Root  Fillings.) 

Fractures  involving  the  cementum  demand  either  the  removal  of 
the  loosened  piece  and  the  construction  of  a  special  crown  retaining 


Fig.  207 


Fig.  2(;8 


Fracture  witli  dovetails  for  amalgam.  (Evan.s.) 


Fig.  269 


Fraccure  of  portion  of  upper  cuspid, 
cause  unknown.  (Skiagrapli  by  Vj. 
Ballard  Lodge.) 


Oblique  fracture  of  root,  with  pin  and 
amalgam  for  restoration,  ready  for  crowning. 
Artificial  crown  and  bridge  work.     (lOvans.) 


a  portion  of  the  natural  crown  as  a  base,  or  the  removal  of  all  of  the 
natural  crown  and  the  mounting  of  a  substitute  upon  the  root,  or  the 
parts  may  be  banded,  or  in  case  of  molars  an  all-metal  crown  may 
be  moimted.  In  some  cases  screws  or  a  staple  must  be  placed  in  the 
roots  and  the  parts  restored  with  amalgam. .  If  the  loosened  portion  be 
retained,  oxychloride  of  zinc  or  thin  oxyphosphate  is  to  be  introduced 
into  the  joint  after  appropriate  sterilization  and  before  the  gold  crown 
is  set.  Should  the  pulp  be  vital  at  the  time  of  fracture,  it  will  l)ecome 
inflamed  and  should  be  removed  by  the  pressure  method  if  possible. 
To  accomplish  this  the  parts  must  be  lashed  together  and  an  occlusal 
opening  made.  After  devitalization  the  parts  may  be  given  a  dove- 
tailed form,  and  be  temporarily  held  together,  internally,  by  amalgam. 
The  requirements  vary,  and  must  have  due  consideration. 


CHAPTER    X. 

STAINS  OF  THE  ENAMEL  AND  DENTINE. 

Certain  stains  are  found  upon  the  surface  of  the  enamel  and  some- 
times penetrating  its  substance.  The  calculus  sometimes  located  upon 
the  enamel  is  not  mcluded  in  this  consideration,  though  the  calculus 
itself  sometimes  becomes  stained.  So  far  as  they  have  been  observed, 
stains  may  be  divided  into  those  of  metallic  and  non-metallic  origin. 

METALLIC  STAINS. 

Metallic  stains  are  those  which  are  caused  by  the  direct  deposition 
of  minute  particles  of  metal,  inhaled  by  workers  in  the  metals,  in  the 
organic  collections  upon  the  surfaces  of  the  teeth,  or  taken  into  the 
mouth  in  various  solutions  of  drugs. 

Copper. — Miller  found  that  "workers  in  copper,  brass,  or  bronze 
all  presented  a  green  stain  upon  the  upper  teeth,  showing  every  shade 
of  green  and  bluish  green  up  to  bluish  purple.  The  latter  color  pre- 
dominated in  rooms  where  phosphor-bronze  was  worked."  Attention 
is  called  to  the  fact  that  "trumpeters  very  often  show  a  discoloration  of 
the  teeth."  Similar  discolorations  are  sometimes  noted  in  proximity 
to  copper  amalgam  fillings.  The  presence  of  copper  was  demonstrated 
in  scrapings  from  some  of  the  stained  teeth,  imparting  a  characteristic 
green  color  to  a  Bunsen  flame. 

Iron. — "Workers  in  iron  presented  stains  of  a  brownish  color." 
As  pointed  out,  "the  green  salts  of  iron  under  the  conditions  found 
in  the  mouth  would  became  oxidized  and  brownish  in  color."  The 
administration  of  iron  salts,  medicinally,  is  believed  to  produce  black 
discolorations,  iron  sulphide  being  formed.  "Iron  deposits  are  usual 
in  the  border  line  between  carious  and  normal  dentine."  It  is  usually 
believed  that  the  brownish  spots  frequently  seen  in  connection  with 
incipient  or  arrested  caries  of  the  underlying  enamel  are  due  to  the 
formation  of  iron  salts. 

Manganese. — Manganese  was  found  in  the  dark-colored  deposits 
upon  the  teeth  of  herbivorous  animals,  but  as  yet  not  upon  those  of 


METALLIC  STAINS  297 

man.  The  investigator  stated  "that  alkaUne  saHvamay  be  necessary 
to  the  pro(hiction  of  these  deposits."  Manganese  stains  may  occur  from 
the  use  of  potassium  permanganate,  manganic  oxide  being  formed. 

Mercury. — In  cases  of  prolonged  mercurial  administration  the 
deposits  (black)  upon  the  teeth  may  give  the  reaction  for  mercury. 
"If  mercury  and  potassium  iodide  are  given  together,  the  green  iodide 
of  mercury  might  be  present  upon  the  teeth."  It  is  probable  in  these 
cases  that  another  discoloring  substance  may  form.  There  is  in 
mercurialisin  more  or  less  gingivitis;  the  gums  are  swollen  and  spongy, 
bleeding  readily.  "More  or  less  putrefactive  decomposition  of  the 
albuminous  matter  present  upon  the  teeth  occurs,  and  hydrogen 
sulphide  is  formed.  Reacting  upon  the  oxyhemoglobin  of  the  blood, 
sulphomethemoglobin  is  formed — greenish  red  in  concentrated, 
green  in  dilute  solutions."  Miller  ascribes  the  discoloration  found  in 
conditions  of  gingivitis  from  various  causes,  with  lack  of  hygienic  care, 
to  a  probable  reaction  between  hydrogen  sulphide  and  oxyhemoglobin. 

Lead. — Ilirt  (quoted  by  Miller)  found  in  cases  of  lead  poisoning 
discolorations  upon  the  teeth:  dark  brown  at  the  necks,  light  brown 
on  the  crowns,  with  sometimes  a  trace  of  yellowish  green.  IVliller's 
tests  (limited  in  number)  showed  no  lead  reaction  from  the  dental 
deposits  in  lead  poisoning. 

Nickel. — Some  of  the  salts  of  nickel  are  green.  "Metallic  nickel 
attacked  by  fluids  of  the  mouth  and  mixtures  of  bread  and  saliva  pro- 
duce greenish  salts.  The  entire  root  of  a  tooth  containing  a  nickel 
retaining  screw  has  been  stained  a  uniform  apple  green. 

Silver. — The  dentine  of  pulpless  teeth  containing  amalgam  fillings 
is  sometimes  stained  black,  owing  to  the  formation  of  silver  sulphide. 

The  use  of  silver  nitrate  as  a  wash  may  cause  the  albuminate  of 
silver  to  precipitate  salts  of  silver  upon  the  teeth.  If  a  cavity  be 
touched  with  silver  nitrate  and  an  amalgam  filling  be  introduced, 
the  salts  of  silver  will  be  instantly  formed  at  any  point  where  the 
silver  nitrate  and  amalgam  combine.  If  this  be  upon  the  enamel,  the 
latter  will  receive  a  somewhat  lasting  black  stain. 

The  nitrate  of  silver  applied  to  dentine  causes  the  dentine  to  assume 
a  light  yellowish  green  tinge,  and  the  allniminate  of  silver  is  formed; 
later  metallic  silver  is  precipitated,  the  tissue  becoming  black. 

Gold. — Gold  chloride  stains  may  be  formed  during  the  bleaching  of 
teeth  containing  gold  fillings  by  the  chlorine  methods.  The  dentine 
becomes  first  pink,  then  violet  or  purple,  then  black.* 

•  Kirk,  American  Text-book  of  Operative  Dentistry. 


298  STAINS  OF  THE  ENAMEL  AND  DENTINE 

NON-METALLIC   STAINS. 

Green  Stain. — This  most  common  of  green  deposits  upon  enamel 
occurs  upon  both  the  temporary  and  the  permanent  teeth,  particularly 
of  young  persons.  The  deposits  usually  have  a  crescentic  form,  are 
mainly  upon  the  labial  faces  of  the  anterior  teeth,  and  may  be  but  a 
narrow  line  or  may  cover  one-half  the  labial  face.  It  is  unusual  for 
the  deposit  to  extend  far  into  the  interproximal  spaces,  their  tendency 
being  to  follow  the  edges  of  the  approximal  surfaces.  While  green  stain 
imdoubtedly  does  form  upon  adult  teeth  (Figs.  270  and  271)  where 
clearly  the  enamel  cuticle  has  long  been  absent,  it  is  only  very 
common  upon  young  teeth  where  remnants  of  Nasmyth's  membrane 
persist  about  their  necks.  The  color  of  these  deposits  varies  from 
light  green  to  greenish  black. 

If  an  instrument  be  passed  over  the  portion  of  enamel  affected, 
more  or  less  roughness  of  the  surface  is  evident.     If  the  deposits  are 

Fig.  270  Fig.  271 


Extension  of  green  stain  on  the  approximal  Extension  of  green  stain  on  the  lingual 

surface  of  the  incisors.     (Miller.)  surface  of  the  incisors.      (Miller.) 

subjected  to  friction  with  abrasives,  they  disappear  slowly  and  the 
enamel  beneath  may  be  found  roughened.  This  has  led  to  the  belief 
that  these  deposits  cause  decalcification  of  the  enamel.  It  is  found 
upon  adult  teeth  that  when  an  area  of  cervicolabial  enamel  has  become 
roughened  through  slight  decalcification,  a  green  stain  is  likely  to 
form  upon  the  rough  surface  if  proper  hygienic  care  be  not  exercised. 
It  is  also  found  that  if  the  stain  be  removed  by  means  of  abrasives, 
the  roughened  enamel  may  be  readily  polished — i.  e.,  the  decalcifica- 
tion is  very  superficial. 

If  cases  be  observed  early  enough  in  childhood,  it  will  be  noted  that 
green  stain  is  usually  j)reccded  by  a  lack  of  oral  hygiene;  collections 
of  food  (Je}>ris  are  not  removed  from  about  the  necks  of  the  teeth, 
which  implies  that  prior  to  the  formation  of  green  stain  the  afi'ected 
enamel  surfaces  have  been  subjected  to  the  action  of  fermenting  food 


NON-METALLIC  STAINS  299 

debris — that  is,  to  acids.  These  facts  have  led  to  an  acceptance  of 
the  view  that  the  roughness  or  decalcification  has  preceded  the  green 
deposits.  "If  teeth  be  placed  in  a  10  per  cent,  solution  of  iiydrochloric, 
acid,  in  from  two  to  four  minutes  the  enamel  cuticle  begins  to  loosen, 
and  in  from  five  to  ten  minutes  is  isolated.  It  is  found  that  the  entire 
stain  comes  away  with  the  cuticle." 

Nature  of  the  Coloring  Matter. — The  coloring  matter  is  found  to 
be  insoluble  in  water,  glycerin,  alcohol,  ether,  chloroform,  and  oil  of 
turpentine.  Mineral  acids,  hydrochloric,  nitric,  and  nitrohydrochloric 
act  but  slowly  upon  the  coloring  matter;  even  hydrochloric  acid 
requires  some  hours  to  completely  destroy  it.  Tincture  of  iodine, 
commonly  believed  to  act  as  a  solvent  of  green  stain,  was  found  to 
affect  it  but  slightly.  Both  chlorine  and  nascent  oxygen  destroy  the 
coloring  matter  rapidly,  the  cuticle  being  bleached  in  a  few  minutes 
by  a  10  per  cent,  solution  of  hydrogen  dioxide.  Thick,  dark-green 
deposits  were  incompletely  bleached  after  eight  hours'  immersion  in 
the  10  per  cent.  HjOj  solution,  pointing  to  a  lack  of  uniformity  in  the 
composition  of  the  stain. 

The  belief  that  the  green  coloring  matter  is  chlorophyll  is  contra- 
dicted by  the  fact  that  it  is  not  soluble  in  ether. 

Miller^  regarded  the  association  of  the  green  discoloration  with 
sulphomethemoglobin,  or  some  allied  substance,  as  the  most  probable 
explanation,  though  he  found  a  micrococcus  in  a  deposit  of  green 
stain  which  produced  a  grayish  green  color  in  glycerin  agar. 

Miller  did  not  find  any  definite  connection  between  a  milk  diet 
and  green  stain. 

Goadby^  has  found  Bacillus  liquefaclens  fluorescens  motilis  present 
in  several  cases  of  green  stain.  It  deposits  in  its  culture  medium  a 
fluorescent  blue-green  pigment.  Other  mouth  bacteria  produce  a 
greenish  pigment — e.  g.,  Bacillus  pyocyaneus  and  Bacillus  fluorescens 
non-liquefaciens."^  The  deposits  of  green  stain  are  considered  to  be 
secondary  to  enamel  tlecalcificatiou  rather  than  the  cause  of  it,  when 
found  in  connection  with  it. 

In  case  of  roughened  enamel,  green  stain  appears  at  times  to  have 
been  taken  into  its  substance,  rendering  removal  without  bleaching 
difficult. 

Black  Stain. — A  peculiar  black  stain  occurs  in  the  mouths  of  appar- 
ently healthy  individuals,  both  men  and  women,  and  smokers  and 
non-smokers,  and  even  with  those  also  who  drink  neither  tea  nor 

»  Dental  Cosmos,  1894.  »  Mycology  of  tlie  Mouth.  '  Ibid. 


300  STAINS  OF  THE  ENAMEL  AND  DENTINE 

coffee.  It  occupies  the  general  position  described  for  green  stain,  but 
may  cover  much  of  the  surface  of  the  teeth.  It  occurs  in  somewhat 
unclean  mouths,  though  the  teeth  may  have  been  regularly  brushed. 
As  a  rule,  those  teeth  having  the  deposit  are  comparatively  free  from 
caries.  Its  etiology  is  not  worked  out,  but  it  may  be  due  to  a  forma- 
tion of  iron  sulphide  in  place  of  sulphomethemoglobin.  It  is  very 
readily  removed,  and  does  not,  as  a  rule,  affect  the  enamel.  At  times 
a  superficial  caries  is  found  associated  with  it,  and  at  some  minute 
spot  the  enamel  may  be  penetrated.  Whether  this  cavity  is  a  result 
of  the  action  of  the  film  is  not  certain. 

Tobacco  Stains. — Smokers  have  characteristic  black  deposits  upon 
both  the  teeth  and  calculus  deposited  upon  them.  The  stain  is  most 
marked  upon  the  lingual  surfaces  of  the  teeth,  and  a  pipestem  held 
well  back  in  the  mouth  may  cause  a  thick  deposit  upon  some  of 
the  posterior  teeth. 

Tobacco  juice  itself  stains  exposed  dentine  and  cementum,  and 
enters  cracks  in  the  enamel,  producing  brown  discolorations  very 
difficult  or  impossible  to  remove. 

Red  Stain. — ^A  peculiar  red  stain  occurs  upon  the  necks  of  some 
teeth,  but  is  not  generally  distributed.  It  is  probably  due  to  chromo- 
genic  bacteria,  as  it  is  only  found  in  unclean  surfaces. 

According  to  Goadby,^  Bacillus  prodigiosus.  Bacillus  rouge  de  Kiel, 
Bacillus  mesentericus  ruber,  Bacillus  roseus,  Sarcina  roseus,  Micro- 
coccus roseus,  and  other  micrococci  produce  a  red  pigment  in  at 
least  some  of  their  media. 

Sarcina  lutea  and  Sarcina  aurantiaca  produce  yellow  and  orange- 
colored  pigment,  respectively.^  The  exact  relation  of  chromogenic 
bacteria  to  stains  is  not  worked  out. 

DENTINE  STAINS. 

Exposed  dentine  may  be  stained  as  enamel  is.  In  addition  it  may 
take  up  certain  stains  like  tobacco. 

Metallic  fillings,  such  as  amalgam,  containing  mercury,  silver, 
copper,  or  cadmium  metals  which  combine  witli  sulphuretted  hydrogen 
to  form  sulphides,  may  cause  staining  of  dentine. 

Metallic  posts  containing  silver,  copper,  or  nickel,  or  made  of 
steel  or  iron  wire,  may  produce  sulphides  in  the  same  manner."  The 
d(>ntine  may  also  be  stained  pink  l)y  liemoglol)in  entering  the  tubules 

»  Mycology  of  flie  Mouth.  2  Jbid. 


TREATMENT  OF  STAINS  301 

during  the  progress  of  venous  hyperemia.     This  finally  develops  iron 
sulphide. 

The  dentine  may  also  be  stained  by  iron  sulphide  formerl  during 
putrefaction  of  the  pulp,  by  the  action  of  ammonium  sulphide  upon  the 
iron  contained  in  the  hemoglobin  of  the  blood  undergoing  decom- 
position. 

TREATMENT  OP  STAINS. 

Enamel  stains  are  best  removed  by  mechanical  means,  after  the 
removal  of  calculus  from  the  teeth.  (See  Salivary  Calculus.)  For  this 
purpose  brush  wheels  and  rubber  cups  charged  with  pumice  and 
revolved  in  the  dental  engine  are  used  to  remove  the  accessible  portions 
of  the  stains.  Next  a  wood  point,  made  by  sharpening  an  orange- 
wood  stick  or  hickory  shoe-peg  to  a  wedge  shape,  is  charged  with 
the  pumice  and  rubbed  by  hand  over  all  the  surfaces  not  reached  by 
the  brushes  and  cups.  For  the  more  inaccessible  situations  the  point  is 
to  be  mounted  in  a  Jack  or  other  porte  polisher.  A  very  fine  linen  tape, 
a  German  silver  strip,  or  floss  silk  charged  with  pumice  will  remove  the 
stains  at  the  contact  points.  A  very  small  finishing  bur  or  dull  ordi- 
nary No.  1  or  No.  ^  bur  is  useful  upon  lingual  surfaces  or  in  grooves. 

The  powdered  pumice  used  is  best  mixed  with  glycerin  to  prevent 
the  flying  of  the  })umice  during  the  rapid  revolution  of  the  wheels. 
Saturation  of  the  stains  with  tincture  of  iodine  renders  them  more  visi- 
ble and  also  brings  to  view  the  associated  bacterial  films  upon  the 
teeth. 

Register  recommends  the  use  of  1  per  cent,  hydrogen  dioxide,  to 
be  forcibly  sprayed  upon  the  gums  and  deposits  both  before  and  after 
the  use  of  tincture  of  iodine.  The  brush  and  pumice  will  then  rapidly 
remove  the  stains  and  bacterial  films  upon  the  accessible  portions 
of  the  teeth. 

Tobacco  stains  in  cementum  need  not  be  removed  to  their  full  depth. 

Head'  has  suggested  the  removal  of  deep  enamel  stains  and  the 
deposits  in  irregular  depressions  and  joints  of  inlays,  inaccessible  to 
the  stick,  by  the  use  of  nascent  oxygen  derived  from  25  per  cent, 
ethereal  pyrozone,  or  a  paste  of  sodiimi  dioxide  and  water,  made  by 
dissolving  the  latter  in  distilled  water  at  about  32°  F.  These  are 
applied  to  the  part  on  cotton,  and  nascent  oxygen  liberated  witli  a 
hot  burnisher.  The  face  and  gums  are  protected  by  the  securely 
placed  rubber  dam  and  by  oiling  the  face. 

»  Items  of  Interest,  1902. 


302  STAINS  OF  THE  ENAMEL  AND  DENTINE 

The  method  is  also  appHcable  to  the  bleaching  of  obstinate  stains 
of  the  dentine,  especially  near  the  cutting  edges. 

In  the  joints  of  inlays  fresh  cement  is  to  be  rubbed — preferably 
Ascher's — in  order  to  prevent  a  rediscoloration. 

If  beneath  green  stains  decalcification  be  discovered,  the  decalcified 
area  should  be  removed,  the  enamel  polished,  and  the  patient  urged 
to  careful  prophylaxis. 

After  the  removal  of  calculus  and  stains  from  the  teeth  the  mouth 
and  teeth  should  be  kept  in  as  cleanly  and  aseptic  a  state  as  possible 
by  the  employment  of  correct  prophylactic  measures.  Dental  caries 
and  pyorrhea  alveolaris  are  thus  also  largely  prevented.  (See  Prophy- 
laxis of  Dental  Caries  and  Pyorrhea  Alveolaris.) 

The  stains  found  in  the  dentine  are  also  divisible  into  metallic  and 
non-metallic.  The  former  are  best  removed  by  transforming  the 
insoluble  metallic  salt  into  a  soluble  one. 

The  most  frequent  and  practicable  course  is  to  form  soluble  chlorides 
through  the  action  of  nascent  chlorine.  Copper,  nickel,  gold,  and  iron 
stains  should  be  subjected  to  the  chlorine  method  of  bleaching, 
followed  by  repeated  washings  with  chlorine  water,  50  per  cent.,  and 
hot  distilled  water  to  remove  the  chloride  formed.^ 

Silver  stains  are  converted  into  silver  chloride  by  the  chlorine  method, 
or  iodide  by  the  use  of  tincture  of  iodine,  and  dissolved  out  by  the  use 
of  sodium  hyposulphite  followed  by  hot  distilled  water.^ 

For  mercurial  stains  Kirk  recommends  the  use  of  aqueous,  ammo- 
niacal  solution  of  hydrogen  dioxide  after  the  chlorine  method,  and  a 
saturated  solution  of  potassium  iodide  after  the  iodine  method,  in 
either  case  followed  by  washing  with  hot  distilled  water. 

Manganese  stain  is  removable  by  the  use  of  25  per  cent,  aqueous 
solution  of  hydrogen  dioxide  saturated  with  oxalic  acid  crystals  and 
followed  by  washing  with  hot  water. 

The  non-metallic  dentine  stains  are  removable  by  the  use  of 
chlorine  evolved  from  chlorinated  lime  by  the  reaction  with  dilute 
acetic  acid,  or  of  nascent  oxygen  evolved  from  hydrogen  dioxide  or 
sodium  dioxide. 

In  either  case  the  color  molecule  is  destroyed  l)y  the  indirect  or 
direct  oxidizing  effect. 

The  hydrogen  dioxide  may  be  used  in  the  form  of  the  25  per  cent, 
ethereal  solution  (25  percent,  pyrozonc)  aj)plicd  for  a  time  or  sealed 
within  the  tooth  for  twenty-four  hours,  or  the  25  per  cent,  aqueous 

'  Kirk.  2  Ibid. 


TREATMENT  OF  STAINS  303 

solution  may  hv  driven  into  the  tubnli  by  tlie  aid  of  the  cataphoric 
current. 

Sodium  dioxide  .should  be  employed  in  .saturated  .solution  in  di.stilled 
water  (made  at  about  32°  F.).  The  dentine  i.s  first  desiccated  and 
then  saturated  with  the  solution.  Weak  sulphuric  acid  (10  per  cent.) 
is  used  to  liberate  the  nascent  oxygen.  Kirk  recommends  a  second 
application,  omitting  the  use  of  the  acid. 

As  with  metallic  stains,  all  the  by-products  should  be  washed  out 
with  hot  distilled  water.' 

A  further  description  will  be  given  under  the  caption  of  ^Nloist 
Gangrene  of  the  Pulp. 

'  For  a  completp  (lesfiii>(ioii  of  the  bleaching  process,  see  Kirk's  article  in  American  Text- 
book of  Operative  Dentistry. 


CHAPTER    XL 

DENTAL  CARIES:    HISTORY;  EXCITING  AND   PREDISPOSING 

CAUSES. 

Definition. — Dental  caries  may  be  defined  as  a  disease  of  a  tooth 
characterized  chiefly  by  the  production  of  a  locahzed  cavity,  concavity, 
or  area  containing  decalcified  tooth  structure  and  due  to  a  combined 
acid  fermentation  and  liquefaction. 

History. — Examinations  of  crania  show  the  disease  to  be  certainly 
as  old  as  semicivilization,  and  when  more  data  are  obtainable  it 
will,  no  doubt,  be  found  even  older.  The  skull  of  a  mummy  in  the 
British  Museum,  dating  2800  B.C.,  exhibits  well-marked  caries  and 
other  dental  diseases.  Caries  appears  in  the  teeth  of  the  skulls  of 
all  peoples,  no  matter  what  their  degree  of  civilization,  provided 
their  dietary  included  cooked,  starchy  foods. 

Causes. — ^These  may  be  divided  into  exciting  and  predisposing. 

Prior  to  the  investigations  of  Miller,^  published  in  1882,  a  vast 
amount  of  labor  was  expended  in  the  effort  to  determine  the  cause 
of  dental  caries.  The  deductions  made  were  partly  speculative  and 
partly  based  upon  scientific  investigations. 

From  1754  to  1835  caries  was  regarded  as  an  inflammation  or 
gangrene  of  tooth  structure;  Boudett,  Jourdain,  Hunter,  Fox,  Bell, 
Fitch,  and  Koecker  advancing  one  or  the  other  theory.^ 

In  1835  Robertson,"*  of  Birmingham,  England,  advanced  the  opinion, 
based  upon  his  observations,  that  it  "is  to  chemical  and  not  to  inflam- 
matory action  that  the  destruction  of  the  teeth  must  be  attributed." 
The  author  pointed  out  forcibly  the  errors  and  fallacies  of  previous 
writers.  He  stated  that  "Particles  of  food  retained  in  fissures  and 
imperfections  of  the  teeth  and  in  the  spaces  between  the  teeth  undergo 
a  process  of  decomposition  and  acquire  the  property  of  corroding, 
disuniting,  and  therefore  destroying  the  earthy  and  animal  substances 
of  which  the  teeth  are  composed." 

John  Tomes,  a  little  later,  was  the  first  to  record  microscopic  exam- 

'  International  iJcnt.al  Journal,  1884. 

2  For  an   interesting  and  exhaustive  exposition  of  their   views,   see  American   System  of 
Dentistry,  .Section  on  Dental  Pathology,  by  Black. 

'  A  Practical  Treatise  on  the  Human  Teeth,  second  edition,  Philadelphia,  1839. 


HISTORY  AND  EXCITING  CAUSES  305 

inations  of  carious  dentine.  He  described  the  transparent  zone  lying 
between  the  carious  and  non-carious  dentine,  and  observed  and 
pointed  out  also  the  dentinal  fibrillar.  He  announced  the  very 
significant  fact  in  relation  to  caries,  that  if  blue  litmus  paper  be  applied 
to  a  carious  cavity  it  is  at  once  reddened,  which  furnishes  evidence 
of  the  presence  of  an  agent  capable,  if  unresisted  by  the  vitality  of 
the  dentine,  of  depriving  the  tissue  of  its  earthy  constituents,  leaving 
the  "gelatin  to  undergo  a  gradual  decomposition  favored  by  the  heat 
and  moisture  of  the  mouth." 

Tomes  first  established  the  essentially  chemical  character  of  some 
features  of  caries.  The  character  of  the  acid  and  its  localization  were, 
however,  not  ascertained. 

In  1867  Bridgman  promulgated  the  theory  that  the  crown  of  the 
tooth  and  the  gum  were  of  different  electrical  potential,  and  that  being 
bathed  in  the  oral  fluids  the  conditions  of  a  battery  were  set  up. 

Acid  substances  were  said  to  be  set  free  at  the  positive  pole  (the 
crown),  causing  decalcification. 

S.  B.  Palmer,  in  1874,  claimed  that  after  filling  recurrent  caries  was 
caused  by  the  conditions  of  a  battery  being  set  up — i.  e.,  the  difference 
of  electrical  potential  between  the  filling  and  dentine  in  the  presence 
of  saliva  or  of  the  fluid  of  the  dentine  as  an  electrolyte  caused  liberation 
of  acids,  producing  decalcification  of  the  tooth  or  disintegration  of 
the  filling— e.  g.,  oxy phosphate. 

Miller,  in  1881  and  1900,^  experimentally  examined  these  assump- 
tions. He  ground  the  enamel  away  from  the  crowns  of  freshly  ex- 
tracted teeth  and  filled  cavities  made  in  them  with  gold  and  gutta- 
percha. These  he  placed  in  separate  flasks  containing  a  physiological 
salt  solution  (0.75  per  cent,  table  salt).  This,  in  the  presence  of  electric 
currents,  should  produce  hydrochloric  acid  by  liberation  of  hydrogen 
and  chlorine,  and  decalcification  should  occur.  After  four  years 
there  was  no  decalcification. 

Similarly  filled  teeth  were  suspended  in  dilute  lactic  acid.  The 
decalcification  was  exactly  similar  to  that  in  the  unfilled  pieces  used 
as  a  control.  Had  electrolytic  currents  been  generated  between  the 
metals  and  dentine,  the  latter  would  have  been  acted  upon  more  vigor- 
ously than  in  the  unfilled  pieces. 

In  1868  Watt^  advanced  the  theory  that  free  sulphuric,  nitric,  and 
hydrochloric  acids  were  generated  in  the  mouth  during  putrefactive 
processes  and  caused  the  different  varieties  of  caries. 

>  Dental  Cosmos,  April,  1901.  *  Chemical  Essays,  1868. 

20 


306  DENTAL  CARIES 

Magitot^  pointed  out  that  the  essential  phenomena  of  caries,  as  they 
were  then  understood,  were  the  same  in  natural  teeth  mounted  upon 
plates  as  in  the  natural  organs  in  situ;  proving  that  caries  is  intrinsi- 
cally independent  of  the  existence  of  vitality.  By  immersing  teeth  in 
solutions  of  sugar  undergoing  fermentative  changes  he  found  that 
decalcification  occurred.  Teeth  immersed  in  solutions  of  sugar  in 
which  fermentation  had  been  prevented  by  boiling  the  solution  and 
sealing,  or  by  additions  of  sufficient  carbolic  acid,  remained  unaffected. 

Leber  and  Rottenstein,  in  1867,  first  called  attention  to  the  probable 
causative  association  of  bacteria  with  some  phases  of  dental  caries. 
3y  staining  carious  dentine  with  iodine  the  dilated  dentinal  tubules 
were  shown  to  be  filled  with  granular  bodies,  which  they  recognized  as 
bacteria,  identifying  but  one  of  the  many  forms  of  oral  bacteria — the 
leptothrix.  They  deemed  an  initial  exposure  of  dentine  a  necessary 
preliminary  to  the  invasion  and  growth  of  the  leptothrix,  which  in 
conditions  of  lessened  resistance  gained  access  to  the  tubules  and  in 
some  undescribed  manner  caused  their  dilatation. 

The  question  of  the  recognition  of  the  presence  of  bacteria  directly 
resolves  itself  into  the  subject  of  special  staining.  Prior  to  the  work 
of  Koch,  presented  in  1881,  no  means  of  isolating  specific  bacteria  by 
special  cultures  and  staining  were  known,  and  it  is  remarkable  that  in 
the  same  year  the  essential  features  of  dental  caries  were  first  made 
out  with  some  degree  of  clearness. 

Miles  and  Underwood  (World's  Medical  Congress,  1881)  point  out 
clearly  and  at  length  the  different  appearances  produced  by  simple 
decalcification  of  dentine  and  those  by  dental  caries.  Speaking  of 
Magitot's  experiments,  they  say:  "We  assume  that  two  factors  have 
always  been  in  operation:  (1)  the  action  of  acids  and  (2)  the  action  of 
germs.  When  caries  occurs  in  mouths  it  is  always  under  circumstances 
more  favorable  to  the  action  of  germs  than  to  the  action  of  acids." 
They  I^elieved  that  the  acids  necessary  for  the  decalcification  were 
excreted  by  the  germs,  which  utilized  the  dentinal  fibrillse  as  a  food 
supply. 

It  will  be  seen  that  the  invasion  and  multiplication  of  organisms  in 
the  tubuH  were  held  as  the  antecedent  of  the  process  of  decalcification. 
The  deductions  of  these  gentlemen  were  drawn  from  data  not  derived 
from  the  methods  of  modern  bacteriology — i.  e.,  special  stains  and 
special  cultures.  Moreover,  they  were  made  before  the  physiological 
chemistry  of  bacteria  was  even  partially  understood. 

'  Treatise  on  Dental  Caries,  Experimental  and  Therapeutical  Investigations. 


HISTORY  AND  EXCITING  CAUSES  307 

In  1882  W.  D.  Miller,  of  Berlin,  announced,  as  the  results  of  experi- 
ments conducted  by  him,  that  he  believed  the  first  stage  of  dental  caries 
to  consist  of  a  decalcification  of  the  tissues  of  the  teeth  by  acids  which 
are  for  the  greater  part  generated  in  the  mouth  by  fermentation.  This, 
it  will  be  seen,  is  a  position  in  agreement  with  that  of  Robertson. 

Miller's  observations  and  experiments  established  the  following 
basal  facts  in  connection  with  dental  caries: 

1.  That  in  all  cases  of  dental  caries  microorganisms  may  be  seen 
under  the  microscope  in  the  tubules  of  the  carious  dentine,  and  that 
bacteria  exist  in  great  numbers  in  the  mouth. 

2.  That  the  invasion  of  the  tubules  is  always  preceded  by  decalci- 
fication of  the  dentine — i.  e.,  an  area  sometimes  relatively  large  of 
decalcified  dentine  may  be  seen  in  advance  of  the  organisms. 

3.  Analysis  of  the  softened  dentine  proved  that  a  large  part  of  its 
lime  salts  were  removed — i.  e.,  decalcification  had  occurred. 

4.  Test  with  litmus  paper  gave  the  acid  reaction  in  nearly  every 
case,  so  that  the  inference  that  decalcification  was  due  to  an  acid  was 
warrantable. 

5.  The  food  substances  taken  into  the  mouth  are  of  all  classes. 
Carbohydrates  (sugars  and  starches),  hydrocarbons  (fats),  and  nitrog- 
enous (albuminous)  materials. 

The  carbohydrates  are  fermented  with  acid  reaction  by  many  mouth 
bacteria,  commonly  producing  lactic  acid;  the  albumins  ferment  with 
an  alkaline  reaction. 

It  was  inferred  from  this  and  other  experiments  that  caries  was  due 
to  the  acid  fermentation  of  carbohydrates  and  not  directly  to  the 
fermentation  of  albuminous  substances. 

6.  That  oral  fermentation  is  the  result  of  bacterial  action  his  follow- 
ing fundamental  experiments  show : 

(a)  A  small  tube  was  filled  with  a  solution  of  starch  and  fastened 
to  a  molar  tooth  on  retiring.  The  next  morning  the  contents  of  the 
tube  had  a  strong  acid  reaction.  A  tube  of  the  starch  sohition  with 
saliva  added  was  incubated  at  blood  temperature.  After  four  or  five 
hours  the  mixture  became  acid. 

(b)  The  mixture  of  starch  and  saliva  was  kept  at  100°  C.  for  a  half- 
hour  and  incubated.  It  did  not  become  acid — /.  e.,  the  exposure  to 
this  temperature  killed  the  ferment. 

(c)  The  saliva  was  boiled  for  a  half-hour  and  then  added  to  the 
starch  solution  and  the  mixture  incubated.  No  acid  was  produced — 
i.  e.,  the  ferment  existed  in  the  saliva,  not  in  the  starch. 


308  DENTAL  CARIES 

(d)  The  ptyalin  of  the  sahva  was  destroyed  by  heating  the  mixture 
for  twenty  minutes  at  67°  C. ;  the  incubated  mixture  still  became  acid 
— i.  e.,  ptyalin  did  not  act  as  the  acid-forming  ferment,  but  the  fermen- 
tation must  have  been  caused  by  some  other  ferment  not  destroyed  by 
exposure  to  this  temperature. 

(e)  To  the  mixture  of  saliva  and  starch  carbolic  acid  was  added 
as  an  antiseptic.  No  acid  was  formed,  but  the  ptyalin  changed  the 
starch  to  sugar. 

(J)  A  number  of  tubes  were  each  supplied  with  a  small  quantity  of 
the  saliva-starch  solution  and  sterilized;  a  third  of  them  were  infected 
from  the  mouth,  a  third  by  carious  dentine,  and  a  third  were  left  unin- 
fected as  controls.  The  infected  tubes  became  acid;  the  controls  did  not. 

(g)  The  first  of  a  series  of  tubes  containing  sterilized  saliva  and 
starch  solution  was  infected  with  carious  dentine;  when  this  became 
acid  a  fraction  of  a  drop  was  carried  from  it  to  a  second  tube.  Aftei 
that  became  acid  a  third  was  infected  from  it,  and  so  on  indefinitely. 

Conclusion. — Carious  dentine  contains  a  ferment  or  ferments 
capable  of  reproduction — i.  e.,  living  organisms  are  present  in  it. 

7.  The  nature  of  this  living  ferment  was  determined  by  infecting 
a  culture  medium  with  carious  dentine  taken  from  the  deeper  layers. 
The  bacteria  cultivated  were  distended  into  pure  cultures  by  carrying 
through  a  series  of  cultures  and  examining  microscopically  during 
the  process.  The  same  morphological  characteristics  were  exhibited 
in  the  last  tube  as  shown  by  the  germs  in  the  deeper  layers  of  carious 
dentine  itself,  and  was  identical  with  that  of  bacterium  acidi  lactici. 
These  germs  may  be  found  in  the  sediment  of  a  culture  tube,  and 
consist  of  cocci  and  micrococci,  either  single  or  in  chains.  These 
cocci  possess  the  power  of  forming  lactic  acid  from  glucose.  The 
organism  is  a  facultative  anaerobe  (Fig.  272). 

8.  A  sound  bicuspid  was  sawed  into  sections  and  an  equal  number 
of  these  sections  placed  in  each  of  two  test-tubes.  Upon  these  was 
poured  a  2  per  cent,  aqueous  extract  of  beef  (albuminous).  To  one 
tube  a  minute  portion  (0.2  per  cent.)  of  cane-sugar  was  added.  Both 
tubes  were  sterilized,  and  after  cooling  infected  with  a  pure  culture 
of  the  germ  obtained  from  the  deeper  layer  of  carious  dentine.  The 
sugar-containing  solution  became  acid  in  a  few  hours;  in  a  week  the 
dentine  was  softened;  in  two  weeks  thin  sections  were  completely 
decalcified;  in  three  weeks  cavities  were  found  in  the  dentine  exactly 
similar  to  cavities  formed  in  teeth  in  the  mouth  and  presenting  under 
the  microscope  other  phenomena  of  caries  to  be  described  later. 


HISTORY  AND  EXCITING  CAUSES 


309 


A  more  prolonged  fermentation  resulted  in  the  complete  disintegra- 
tion of  the  slabs  of  dentine,  a  proof  of  the  fact  that  one  organism 
may  completely  destroy  dentine. 

In  the  tube  containing  only  the  extract  of  beef  no  acid  was  pro- 
duced, and  no  decalcification  of  the  dentine  occurred. 

From  these  facts  Miller  argued  that  putrefaction  does  not  initiate 
the  process  of  dental  caries,  and  may  not  be  essential  to  the  destruc- 
tion of  either  the  inorganic  or  organic  dental  elements. 

9.  That  the  acid  produced  was  lactic  acid  Miller  demonstrated  as 
follows : 

Starch  and  saliva  were  mixed  and  fermentation  induced.  This  was 
then  checked  by  stcrihzation  with  heat.  A  quantity  of  material  being 
collectetl  in  this  manner,  the  whole  was  concentrated  by  evaporation 


Fig.  272 


Fig.  273 


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and  tested  with  a  solution  of  methyl  violet,  which  would  turn  first 
blue  and  then  green  with  an  inorganic  acid.  Not  so  reacting,  and  not 
distilling  off  during  the  concentration,  the  acid  present  was  pronounced 
a  non-volatile  organic  acid.  The  concentrate  was  shaken  with  a 
quantity  of  ether,  which  dissolved  the  organic  acid  present.  AVhen 
the  solution  was  clear  it  was  filtered  and  the  etlier  partially  distilled 
off,  when  the  partially  concentrated  solution  was  further  concentrated 
over  a  water  bath  and  then  mixed  with  an  excess  of  freshly  prepared 
zinc  oxide.  The  whole  was  boiled,  water  being  added  as  needed, 
until  the  solution  became  neutral,  when  it  was  set  aside  to  crystallize. 
A  drop  placed  upon  a  slide  under  the  microscope  showed  the  forms 
of  crystals  of  zinc  lactate  (Fig.  273). 


310  DENTAL  CARIES 

By  testing  the  molecular  weight  of  the  washed  and  dried  crystals 
it  was  determined  clearly  that  the  substance  was  zinc  lactate. 

In  practically  a  similar  manner  lactic  acid  was  obtained  directly 
from  carious  dentine. 

^Miile  Miller  demonstrated  the  ability  of  one  organism  to  produce 
all  the  essential  phenomena  of  caries,  including  liquefaction  of  the 
dentine,  he  did  not  claim  that  only  one  or  two  organisms  are  involved 
in  the  process,  but  that  "any  germs  possessing  the  power  of  producing 
acid  fermentation  of  food  may  and  do  take  part  in  the  first  stage  of 
caries,  and  that  all  those  possessing  a  peptonizing  or  digestive  action 
upon  albuminous  substances  may  take  part  in  the  second  stage; 
and  that  those  possessing  both  properties  may  take  part  in  both 
stages."^ 

He  was  of  the  opinion  that  it  is  not  the  presence  of  this  or  that  kind 
of  bacterium,  but  rather  the  joint  activity  of  the  total  flora  as  expressed 
in  intensity  of  fermentation  in  food  particles  which  determines  the 
extent  of  caries. 

Out  of  eighteen  mouth  bacteria  examined  Miller  found  ten  that 
produced  lactic  acid  in  sugar-containing  solutions.^ 

Hinkins  and  Acree,^  in  experiments  upon  pure  cultures  of  a  number 
of  oral  bacteria  in  various  artificial  media,  found  lactic,  butyric, 
valerianic,  formic,  carbonic,  and  hydrosulphuric  acids  as  either  prin- 
cipal or  by-products  of  the  fermentation. 

It  is  quite  clear  from  Miller's  demonstrations  that  bacteria,  or  at 
least  one  bacterium,  are  the  exciting  causes  of  dental  caries;  and  that 
for  their  function  as  such  they  require  carbohydrate  material  as  food. 

Their  action  upon  these  substances  has  been  studied.  The  carbo- 
hydrates introduced  into  the  mouth  as  food  are  monosaccharids, 
disaccharids,  and  polysaccharids.  (1)  The  monosaccharids  or 
glucoses  have  the  general  formula  CglljjOg,  and  are  represented  by 
dextrose  and  levulose,  found  in  fruits,  honey,  and  in  many  forms  of 
candy,  such  as  peanut  brittle  and  glacis,  and  galactose  formed  from 
lactose  or  milk  sugar  by  hydrolysis.  These  ferment  directly  into 
lactic  acid  witliout  formation  of  gas. 

CJ-IijOb  +  bacterial  ferment  =  2C3lI„03. 

A  certain  proportion  of  the  glucose,  etc.,  is  appropriated  by  the 
bacteria  as  food.  (2)  Disaccharids  or  saccharoses  have  the  general 
formula  Cj2H220jj.     The  principal  one  is  saccharose  found  in  sugar- 

'  MicroSrganisms  of  the  Human  Mouth.  '  Ibid.  '  Dental  Cosmos,  1901. 


HISTORY  AND  EXCITING  CAUSES  311 

cane,  the  sugar-beet,  sugar-maple,  anrl  maize.  This  is  inverted  by 
the  ferment  of  the  bacteria  into  ghicose  and  levulose  tlirough  a 
process  of  hydration: 

C12H22O11  +  H2O  +  bacterial  ferment  =  CeH^^O,  +  C,Hi,Oe. 

Two  other  disaccharids  enter  the  mouth  or  are  formed  therein: 
lactose  and  maltose,  both  Cj2H220jj(H20).  Lactose  exists  in  milk 
and  by  hydrolysis  is  changed  to  galactose,  2C(jHj20p,  and  then  fer- 
ments like  other  monosaccharids.  Maltose  is  an  intermediate  product 
in  the  formation  of  glucose  from  starch,  and  is  produced  by  the 
action  of  ptyalin.  (3)  Polysaccharids  or  amyloses  with  the  general 
formula  (QHjoOj)  n.     Starch,  cellulose,  glycogen,  and  gum. 

Starch  was  found  by  Miller  not  to  undergo  direct  fermentation  by 
mouth  bacteria — i.  e.,  culture  media  containing  starch  but  not  sugar 
when  infected  by  bacteria  did  not  ferment  into  lactic  acid  unless 
ptyalin  was  present.^  When  saliva  was  used,  however,  the  acid 
reaction  occurred,  owing  to  the  formation  of  maltose  through  the  action 
of  ptyalin. 

In  oral  fermentation  starch  is  first  changed  to  maltose  by  hydration; 
and  the  maltose  to  lactic  acid : 

2QH,„0,  +  2H2O  +  ptyalin  =  C,2H220,,(H20). 

Starch.  Water.  Maltose. 

CJI,,0,,i}iJ3)  +  bacterial  ferment  -  4C3H8O3. 

Maltose.  Lactic  acid. 

According  to  Goodby^  a  few  bacteria  found  in  the  mouth  can  produce 
the  change  direct.  This  is  of  no  practical  consequence,  however, 
as  ptyalin  is  always  present. 

Glycogen,  CgHj^Og,  or  animal  starch,  is  femiented  to  gluco.se  by 
liver  cell  ferment,  and  probably  exists  in  the  oral  epithelium  in  cer- 
tain states  as  well  as  in  the  saliva  in  others.  (See  Glycogenic  Infiltra- 
tion and  pages  321  and  322.) 

Miller  has  demonstrated  that  bacteria  produce  acid  from  starches 
and  sugars  in  about  equal  proportions,  provided  the  starches  are 
cooked.  The  cooking  of  starchy  foods  bursts  the  starch  granules 
and  renders  them  more  adhesive  to  the  teeth,  as  well  as  more  fer- 
mentable. The  following  synopsis  of  experiments-^  made  with  food 
mixed  with  .saliva  in  definite  quantities  speaks  for  itself: 

'  American  System  of  Dentistry,  vol.  i,  p.  805. 

2  Mycology  of  the  Mouth. 

'  Microorganisms  of  the  Human  Mouth. 


312  DENTAL  CARIES 

Matenal.  Duration  of  experiment.  Acid  formed,  in  unita.^ 
Bread,  starch,  potato,  maccaroni, 

rice,   com,   and   other    cooked 

starches 12  and  30  hours.  20  to  25  and  42  to  110 

Raw  starches,  potato,  spinach,  etc.  "             •"        "  q                         q 

Cane-sugar  and  grape-sugar  .      .  "             "        "  17  to  20  and  37  to    41 

Meats,  fish,  eggs,  etc "            "       "  0  or  alkaline 

The  table  shows  that  albuminous  materials  and  raw  starches 
produce  no  acid  and  are  not  concerned  in  caries  except  in  so  far  as 
meats,  etc.,  act  as  culture  media  perpetuating  bacteria  which  later 
may  produce  an  acid  reaction  in  carbohydrate  materials. 

The  fats  may  be  fermented  with  production  of  fatty  acids.  Goadby 
has  found  these  of  no  importance  in  relation  to  caries,  but  Miller  has 
shown  that  the  acids  found  in  dermoid  cysts,  among  which  are 
fatty  acids,  can  produce  decalcification;  as  other  acids,  as  oxalic, 
were  present,  the  relation  of  fatty  acids  is  not  quite  clear.  Miller 
asserts  that  fats  deposited  upon  the  teeth  as  well  as  calculus  retard 
decay,  and  that  fat  mixed  with  saliva  will  give  an  alkaline  reaction.^ 

That  alkalies  do  not  produce  tooth  disintegration  in  the  mouth  is 
shown  by  the  fact  that  a  tooth  is  not  affected  by  alkaline  solutions 
which  are  not  strong  enough  to  injure  the  soft  parts. 

The  influence  of  carbohydrate  diet  in  the  production  of  caries  is 
well  shown  by  tables  compiled  by  Mummery  and  quoted  by  Miller.^ 
The  races  consuming  a  fish  and  meat  diet  almost  exclusively — e.  g., 
the  Esquimaux — are  recorded  as  having  about  3  per  cent,  of  caries 
in  skulls  examined,  while  those  using  a  mixed  or  vegetable  diet  have 
from  10  to  40  per  cent,  of  caries.  A  most  convincing  example  is 
that  given  by  Miller  of  two  related  tribes  living  on  either  side  of 
the  Andes,  in  the  Argentine  Republic  and  Chili,  respectively.  The 
former,  a  cattle-breeding  and  meat-eating  tribe,  were  practically  free 
from  caries,  while  the  latter,  living  on  mixed  foods  and  consuming 
sugar,  had  19  per  cent,  of  caries. 

While  the  fermentation  of  carbohydrate  food  debris  into  acid  is 
conceded  to  be  the  active  exciting  cause  of  dental  caries,  the  modus 
operandi  of  the  inception  has  not  been  satisfactorily  settled.  Miller 
holds  that  as  he  was  able  to  find  bacterial  plaques  upon  many  sur- 
faces of  teeth,  even  in  the  mouths  of  immunes  without  caries  beneath, 
the  plaques  had  no  relation  to  the  inception  of  caries  of  enamel,  but 
that  the  carbohydrate  food  collecting  at  favoring  spots  undergoes  acid 
fermentation,  with  production  of  enamel  decalcification,  after  which 

1  An  aoJd  unit  equals  the  amount  of  acid  necessary  to  neutralize  0.1  c.c.  of  a  0.5  per  cent, 
solution  of  potassium  hydrate— i.  e.,  0.20  c.c.  of  the  latter  used  equals  twenty  acid  units. 

2  Dental  Co.smos.  1904.  '  Microorganisms  of  the  Human  Mouth. 


HISTORY  AND  EXCITING  CAUSES  313 

the  bacteria  enter.  By  experiments  he  determined  that  the  plaques 
rather  hindered  the  action  of  acids  experimentally  used  as  a  decal- 
cifying agent.  Black,  on  the  other  hand,  claims  that  the  bacteria 
produce  a  gelatinoid  material  and  are  left  upon  the  teeth  in 
the  form  of  a  plaque  or  zooglea  mass,  and  that  the  plaque  is  a 
thin,  transparent,  slightly  yellowish  film  not  seen  without  close  in- 
spection. Williams  found  a  film  of  bacteria  over  the  decalcified 
area  in  almost  all  cases  of  superficial  caries  of  enamel,  and  that  it 
has  sufficient  resistance  to  permit  grinding  in  situ  (Figs.  289  and  290). 

Goodby  frequently  found  on  the  opaque  white  patches  of  softened 
enamel  a  coccus  to  which  Williams  called  attention  which  would  cause 
a  plaque  deposition  upon  teeth  suspended  in  its  culture,  and 
that  when  acid-producing  bacteria  were  mixed  with  the  coccus 
and  a  carbohydrate  medium  used,  superficial  decalcification  of  the 
enamel  under  the  plaques  was  produced  in  from  a  week  to  ten  days. 

Miller  also  showed  that  in  the  immune  with  unclean  teeth  the 
putrefactive  reaction  was  the  dominant  one,  and  that  the  collection,  if 
persistent,  could  act  as  a  protective  against  the  access  of  acid- 
producing  material. 

In  the  above  data  we  find  that  the  plaques  are  almost  universal, 
even  on  immune  surfaces  (Miller),  so  that  their  presence  on  a  decal- 
cifying surface  is  probably  true,  as  claimed  by  A^'illiams.  If,  then,  they 
are  a  protection  against  the  acids  produced  from  carbohydrate  they 
should  protect,  but  they  do  not.  Secondly,  experiments  with  formed 
acids  are  not  conclusive,  as  they  may  even  be  germicidal  and  the 
dead  film  might  be  a  relative  protection  against  decalcification  by 
the  acids.  The  bacterial  films,  if  containing  acid-producing  bacteria, 
can  easily  take  up  any  carbohydrate  food  collected  against  them,  form 
acid  from  it  which  they  then  pass  to  the  enamel,  hold  it  against  it  and 
permit  it  to  abstract  the  calcium  salts,  which  they  then  pass  out  as 
lactates,  etc.,  or  allow  to  remain  in  situ.  This  latter  conclusion  in  the 
main  is  the  theory  of  Black,  and  while  the  decalcifying  ability  of 
infected  carbohydrate  food  without  the  intervention  of  the  plaques 
is  a  possibility,  it  seems  a  reasonable  conclusion  to  admit  the 
activity  of  the  plaques. 

The  frequent  disturbance  of  the  plaques  by  monthly  cleansings  also 
prevents  dental  caries  in  large  degree,  so  that  they  must  have  some 
relation  to  the  inception,  though  it  is  only  fair  to  state  that  a  constant 
warfare  against  any  species  of  bacteria  doubtless  vastly  reduces  their 
number  in  the  mouth. 


314  DENTAL  CARIES 

The  Predisposing  Causes  of  Caries. — The  causes  of  the  predis- 
position to  caries  are  local  and  general. 

Local  Predisposing  Causes. — So  invariably  does  caries  begin  in  sulci 
or  pits  upon  approximal  surfaces,  about  defective  fillings,  and  upon 
unclean  surfaces,  that  faults  of  form  or  retentive  nature  of  approxima- 
tion, defects,  and  faulty  position  of  the  teeth  must  bear  a  relation  to  the 
difficulty  of  keeping  the  parts  free  from  accumulations  of  bacteria  and 
carbohydrates. 

These  local  predisposing  causes,  as  they  are  called,  are  simply  con- 
ditions favoring  the  formation  of  the  bacterial  plaques  upon  the  teeth 
and  the  retention  of  carbohydrate  food. 

Faults  of  Foem. — Deep  pits  or  sulci  in  the  occlusal  surfaces  of 
bicuspids  or  the  occlusal  or  buccal  surfaces  of  molars,  or  in  the  lingual 
surfaces  of  incisors,  and  occasionally  cuspids,  or  pits  upon  the  cusps 
of  bicuspids  or  molars,  or  in  other  unusual  situations,  are  not  sub- 
jected to  a  cleansing  friction,  and  so  permit  bacteria  to  form  plaques 
in  these  locations  (Fig.  275) . 

The  nature  of  the  approximal  contact  has  to  do  with  the  inception 
of  caries.  Teeth  are  seen  in  which  the  approximal  surfaces  are  well 
rounded  and  their  buccal  and  lingual  angles  free  from  approximation. 
Such  teeth  are  usually  relatively  narrow  at  their  cervices,  so  that 
these  also  recede  well  from  the  line  of  contact.  A  V-shaped  space 
is  formed  which  the  gum  festoon  normally  nearly  fills.  Such  per- 
fection of  contour  is  also,  as  a  rule,  associated  with  a  perfect  organi- 
zation of  the  enamel  structure,  in  virtue  of  which  the  surface  is  smooth. 

^Miile  such  teeth  may  decay  approximally,  there  is  much  less  tend- 
ency to  caries  (Fig.  291). 

Opposed  to  this,  approximations  exist  of  a  broad  nature.  Broad 
approximations  are  very  common  and  not  infrequently  are  associated 
with  a  certain  degree  of  enamel  opacity  and  an  unevenness  of  enamel 
surface  plainly  visible  to  the  naked  eye. 

The  fluid  exuded  by  the  gum  is  normally  alkaline  in  character 
and  probably  neutralizes  the  products  of  acid  fermentation.  In  view 
of  this  fact,  the  first-mentioned  form  of  contact  evidently  affords  more 
of  this  immunizing  principle.  The  extension  of  cavity  margins  beneath 
the  gum  has  been  strongly  indicated  by  experience  as  good  practice, 
and  probably  is  explainable  upon  the  same  ground.  There  is  also 
some  evidence  that  the  gum  has  some  cleansing  action  upon  metal 
placed  beneath  it,  as  it  is  noted  that  when  unclean  gold  crowns  are 
removed  the  portion  extending  beneath  the  gum  is  usually  quite  clean. 


HISTORY  AND  EXCITING  CAUSES  315 

With  the  narrow  approximations  saliva  is  readily  forced  between 
the  teeth  and  neutralizes  the  acids  formed,  or  washes  away  soluble 
carbohydrates,  the  food  for  the  bacteria.  With  the  broad  approxima- 
tions such  a  result  is  less  likely  to  occur. 

Stagnant  saliva  retaining  carbohydrates  probably  will  develop  an 
acid  reaction.      (Miller.) 

A  depressed  approximal  surface  may  decay,  but  frequently  does  not. 
An  acquired  fault  of  form  requires  notice. 

Anatomically  the  gum  covers  the  cementum  and  the  enamel  margin. 
When  recession  of  the  gum  occurs,  the  cementum  is  left  exposed  and 
food  debris  accumulates  at  the  angle  formed  by  it  with  the  gum. 
Owing  to  the  cementum  being  less  smooth  than  enamel,  microbic 
plaques  readily  collect,  hence  decay  of  the  cementum  frequently 
occurs.     (See  Figs.  281  and  285.) 

Arrangement  and  Position  of  the  Teeth. — The  overlapping 
of  one  tooth  upon  another  creates  a  form  of  contact  producing  a 
tendency  to  decay  at  that  point.  Angle^  claims  to  have  observed  a 
comparative  freedom  from  caries  of  very  irregular  teeth  (Fig.  288). 

The  presence  of  a  supernumerary  third  molar  lying  at  the  buccal 
side  of  the  interdental  space  between  the  second  and  third  upper 
molar,  or  an  inlocked  bicuspid,  very  frequently  causes  approximal 
caries  at  the  contact  points.  The  upper  third  and  lower  third  molars 
frequently  stand  in  bad  relation  to  the  cheek  or  the  gum. 

Food  collects  upon  their  buccal  surfaces,  or  they  are  not  subjected 
to  the  friction  of  the  tooth-brush,  and  decalcification  of  a  broad  area 
of  a  buccal  surface  frequently  results. 

Defects  about  Fillings. — Under  the  caption  of  Recurrence  of 
Caries  will  be  found  a  list  of  the  causes  which  perpetuate  caries  about 
fillings.  I  believe  the  abundance  of  these  and  a  lack  of  oral  hygiene 
to  be,  in  a  large  degree,  the  measure  of  a  tendency  to  persistent 
caries.  A  patient  has  a  large  number  of  cavities  due  to  a  period  of 
negligence  with  consequent  intensity  of  oral  fermentation.  If  these 
are  obliterated  in  the  best  manner  with  physically  perfect  fillings,  and 
oral  hygiene  be  exact,  the  tendency  to  caries  is  largely  obliterated.  If, 
on  the  other  hand,  a  large  number  of  even  slightly  defective  fillings 
are  made,  not  only  is  recurrent  caries  induced,  but  the  caries  ferment  is 
continuously  active  and  exact  oral  hygiene  is  an  impossibility.  The 
number  of  cleansings  a  day  is  no  guarantee  of  perfect  hygiene,  even 
with  perfect  teeth,  as  nothing  is  more  common  than  to  see  unclean 

'  Dental  Cosmos,  1903. 


316  DENTAL  CARIES 

embrasures  easily  taking  the  stain  of  tincture  of  iodine  even  in  the 
anterior  part  of  the  mouth  (in  less  degree  than  shown  in  Fig.  274). 
Unquestionably  food  debris  may  even  be  swept  into  the  interdental 
spaces  by  brushing  alone.  Miller^  has  shown  that  a  mixture  of 
bread  and  saliva  may  become  decidely  acid  in  one  hour  and  super- 
ficially decalcify  sections  of  dentine  in  five  hours.  With  this  going  on, 
day  after  day,  in  cases  of  soluble  teeth  and  without  other  aid  than 
brushing,  and  often  this  not  thoroughly  done,  the  persistence  of  decay 
is  not  surprising.  This,  however,  does  not  prove  the  absence  of 
systemic  susceptibility  or  immunity  as  an  added  cause  of  caries  or 
its  absence. 

Other  Local  Predisposing  Causes. — ^Acids  taken  in  excess  into 
the  mouth  may  act  as  predisponents  by  causing  a  roughness  of  the 
enamel,  which  invites  the  formation  of  the  bacterial  plaques.  A 
course  of  tincture  of  ferric  chloride  has  a  bad  reputation  in  this  con- 
nection. In  the  cases  observed  by  the  editor  the  hydrochloric  acid 
in  the  tincture  seemed  to  have  formed  roughnesses  between  the  teeth, 
and  many  large  cavities  of  not  unusual  form  were  later  produced 
and  evidently  due  to  the  carious  process. 

The  acid  vomitus  of  pregnancy  and  seasickness  have  an  analogous 
effect.  It  is  not  likely,  however,  that  during  a  transatlantic  voyage 
large  cavities  can  develop.  The  probable  explanation  of  the  presence 
of  such  cavities  directly  after  the  voyage  is  that  they  existed  before 
the  voyage  was  begun.  Cavities  are  frequently  left  or  overlooked. 
(See  Prophylaxis  of  Caries.) 

Miller  found  that  the  saliva  has  no  antiseptic  quality  as  a  whole 
and  contains  no  antiseptic  substance,  and  though  he  found  the  saliva 
of  immunes  to  develop  a  little  less  acid  than  that  of  highly  susceptible 
individuals,  the  difference  was  not  constant  and  not  sufficient  to 
account  for  the  marked  difference  in  susceptibility.  Miller  found  that 
carbohydrate  foodstuffs  mixed  with  an  alkaline  saliva  became  even 
more  acid  than  when  the  reaction  of  the  saliva  was  intensely  acid 
and  the  chance  for  caries  was  about  the  same  with  either  reaction 
at  the  start. 

Under  conditions  of  oral  irritation,  such  as  catarrhal  stomatitis,  or 
even  the  presence  of  many  cavities  of  decay,  a  stringy,  mucinous  con- 
dition of  the  saliva  may  result.  This  may  be  due  to  a  partial  coagula- 
tion of  the  mucin  by  the  acid  present  in  the  mouth,  and  the  coagulum 
may  entangle  food  masses  and  cause  their  adherence  to  the  teeth. 

'  Dental  Cosmos,  1905. 


HISTORY  AND  EXCITING  CAUSES  317 

The  contention  of  Lohmann  that  the  carbohydrate  element  in 
mucin  was  the  cause  of  caries  Miller  examined  experimentally  and 
found  it  untenable,  but  that  the  explanation  here  given  of  its  entangling 
action  is  the  probable  one. 

Miller  has  noted  that  some  immunes  have  had  exceedingly  ropy 
saliva  which  could  be  drawn  out  into  long  threads,  while  much  caries 
was  noted  in  the  mouths  of  some  almost  absolutely  free  from  mucus. 

He  also  pointed  out  that  the  mucus  may  readily  undergo  putrefactive 
fermentation  with  alkaline  reaction,  and,  again,  the  carbohydrates 
entangled  in  it  will  ferment  with  acid  reaction,  causing  any  caries 
which  might  be  attributable  to  mucin  fermentation. 

It  is  possible  that  the  secretion  from  the  gum  may  in  some  cases 
be  acid  and  favor  the  production  of  caries  by  decalcifying  the  enamel 
about  the  cervix  (Fig.  274). 

Fig.  274 


Caries  of  enamel  about  the  cervices  of  many  teeth,  due  to  tenacious  films  collected  upon 
them;  at  first  probably  neglected,  later  impossible  to  cleanse  with  brush  alone.  (Model  by 
W.  A.  Capon.) 

Cook  has  shown  that  glycogenic  infiltration  of  the  oral  mucous 
membrane  may  be  produced  by  the  use  of  irritant  or  astrigent  washes, 
which  may  possibly  permit  a  change  of  this  substance  by  bacteria  into 
acid  about  the  necks  of  teeth,  accounting  for  a  certain  form  of  cervical 
decay  long  thought  to  be  due  to  an  acid  mucus.  (See  Glycogenic 
Infiltration.) 

Structure. — While  the  structure  of  the  enamel  has  no  relation  to  the 
inception  of  caries,  that  is,  teeth  of  poor  structure  may  not  decay,  a 
roughness  of  the  enamel  surface  may  act  as  a  favoring  condition,  and 
after  inception  of  caries  inferior  structure  and  possibly  the  presence 
of  Caush's  tubes  may  permit  more  rapitl  disintegration.  (See  p.  1G4.) 
An  interesting  examination  of  16,000  mouths  made  in  Sweden  by 
Forberg  (Stockholm)  and  others  by  Rose  in  Baden  and  Thuringia 
seem  to  show  that  there  is  a  relation  between  the  color  (structure)  of 


318  DENTAL  CARIES 

teeth  and  the  presence  of  caries,  the  following  averages  of  all  ages 
being  observed:  white  teeth,  14.3  per  cent,  of  caries;  yellowish  white, 
16.4  per  cent.;  yellow,  20  per  cent.;  grayish  blue  24.3  per  cent. 

According  to  these  observers/  in  the  regions  in  which  the  water  was 
rich  in  calcium  salts  the  individuals  examined  had  the  yellowish  white 
teeth.     Miller's  observations  confirm  this. 

Black"  made  analyses  of  so-called  hard  and  soft  teeth  and  deduced 
from  them  the  opinion  that  the  hardness  and  softness  of  teeth  have 
nothing  to  do  with  the  inception  of  caries. 

Touching  this  point  Black^  instances  the  case  of  a  man  whose 
enamel  had  always  been  chalky  and  as  easily  cut  as  a  slate-pencil, 
yet  who  had  little  caries  of  the  teeth.  That  some  teeth  of  apparently 
poor  structure  and  defective  form  do  not  decay  is  also  a  fact  of  common 
observation,  but,  as  a  rule,  they  go  together. 

These  observations,  together  with  the  foregoing  data,  regarding  the 
inception  of  caries,  point  to  the  now  conceded  conclusion  that  the 
caries  of  teeth  is  entirely  due  to  the  environment  of  the  teeth,  and  in  no 
sense  does  it  arise  from  within  the  tooth,  and  that  in  so  far  as  the  cause 
is  active  it  is  a  question  of  the  localization  of  the  exciting  cause  or  its 
factors  on  the  one  hand,  and  the  solubility  of  the  teeth  on  the  other;  and 
that  no  amount  of  cause  is  sufficient  to  produce  it  unless  permitted 
to  exert  its  effect  upon  special  points  upon  the  teeth;  in  other  words,  it 
requires  localization  and  time  to  act,  though  it  may  in  some  cases  be 
broadly  localized.  There  apparently  remains  only  to  be  considered 
the  effect  produced  by  systemic  states  upon  the  development  of  the 
bacterial  causes  or  whether  any  material  is  introduced  through  the 
oral  juices,  saliva,  mucus,  etc. 

Systemic  Predisposing  Causes. — Some  individuals  seem  to  suffer 
much  from  caries;  others  in  less  degree.  In  either  case  periods  of 
immunity  or  comparative  immunity  may  be  established,  and  may  be 
again  followed  by  a  period  of  susceptibility  and  a  succeeding  immunity. 

These  facts  point  to  the  conclusion  that  a  period  of  caries  is  due 
either  to  a  temporary  lack  of  oral  hygiene  with  a  corresponding 
intensity  in  oral  fermentation — i.  e.,  the  exciting  cause  is  active — or 
that  it  is  due  to  some  systemic  condition  which  changes  the  constitution 
of  the  oral  fluids,  permitting  the  formation  of  the  microbic  plaques 
upon  the  teeth,  or  increases  the  fermentation  by  supplying  some  ele- 
ment nutritive  to  l)acteria  or  depriving  it  of  some  element  inhibiting 
the  growth. 

'  Dental  Cosmos,  1901.  'Ibid,  1898.  'Ibid. 


HISTORY  AND  EXCITING  CAUSES  319 

Black  has  shown  that  caries  fungi  are  always  present  in  the  mouth, 
but  do  not  always  form  the  plaques.  Cases  also  exist  in  which  caries 
has  begun  during  some  period  of  susceptibility  and  a  number  of  new 
cavities  have  been  started.  I^ater  a  period  of  innnunity  has  followed 
and  the  cavities  have  not  progressed. 

So  far  as  classed,  systemic  conditions  influencing  susceptibility  and 
immunity  may  be  placed  under  the  four  headings:  Heredity,  Pre- 
natal and  Postnatal  Influences,  Age,  and  Bodily  Condition, 

Miller  could  find  no  antiseptic  quality  in  the  saliva  nor  any  principle 
corresponding  to  alexin,  and  found  that  bacteria  developed  in  the  saliva 
of  immunes  almost  as  readily  as  in  that  of  those  susceptible  to  caries. 

Heredity. — Black^  records  observations  on  certain  families  as  show- 
ing a  tendency  to  caries  of  certain  teeth  at  a  given  age,  or  in  cer- 
tain positions  upon  the  teeth,  e.  g.,  occlusal  pits.  In  certain  cases  the 
hereditary  tendency  persists.  This  tendency  must  be  due  either  to  an 
inherited  cell  physiology,  or  diet  tendency  influencing  the  oral  fluid, 
or  to  transmitted  faults  of  form  or,  possibly,  of  structure  of  the  teeth. 

Prenatal  and  Postnatal  Influences. — It  is  quite  possible  that  the 
systemic  condition  of  the  mother  during  gestation  may  profoundly 
modify  the  anatomicophysiological  condition  of  the  body  cells  of  the 
child;  nutritional  processes  may  suffer  and  the  postnatal  tooth  develop- 
ment proceed  irregularly,  structure  being  affected;  moreover,  the 
altered  biochemical  function  of  the  cells  may  stand  in  close  relation 
to  the  constitution  of  the  oral  fluids,  and  these  in  turn  may  favor  the 
development  of  caries  fungi.  The  same  line  of  argument  may  be 
applied  to  bottle  feeding  of  recently  born  infants,  or  to  other  con- 
ditions profoundly  affecting  general  nutrition. 

In  an  examination  of  school-children  Th.  Frick"  (Zurich)  found  a 
much  greater  percentage  of  decay  in  children  that  had  been  bottle 
fed  at  between  three  and  six  months  of  age.  He  performed  an  experi- 
ment on  a  litter  of  six  dogs,  feeding  three  on  cows'  milk  and  bouillon; 
one  of  them  died  and  the  others  had  poorly  developed  teeth.  The 
controls  were  normal. 

Forberg  and  Rose^  have  shown  that  the  individuals  who  drink 
water  rich  in  calcium  salts  have  a  smaller  percentage  of  caries  than 
those  drinking  soft  waters.  Whether  this  effect  is  due  to  a  better 
development  of  tooth  structure  or  is  a  postdevelop mental  effect  is 
not  stated.  Degeneracy  must  be  considered  as  a  factor  possibly 
influencing  the  body  cells. 

J  Dental  Cosmos,  1904.  «  Ibid,  1901.  '  Uiiil..  1899. 


320  DENTAL  CARIES 

Age. — That  the  age  has  an  influence  upon  caries  was  noted  by 
Flagg.  He  recorded  the  ages  from  five  to  eight,  twelve  to  twenty, 
thirty  to  thirty-five,  forty-five  to  fifty,  sixty  to  sixty-five,  and  senihty 
as  periods  of  decay,  while  the  intervening  periods  were  intervals  of 
comparative  exemption. 

Black  has  noted  that  caries  is  a  disease  of  youth,  most  intense 
before  adult  age,  at  which  time  immunity  is  established,  provided  the 
teeth  have  been  well  and  promptly  filled  and  the  mouth  otherwise 
cared  for.  In  view  of  this  fact  he  aims  at  establishing  this  immunity 
by  close  attention  to  the  teeth  during  youth. 

He  records  fiuctuations  in  susceptibility  not  unlike  those  recorded 
by  Flagg,  and  also  points  out  that  some  persons  pass  through  the 
ordinary  periods  of  susceptibility  and  first  develop  caries  in  middle 
age.  In  old  age  general  recession  of  the  gum  is  common,  and  in  the 
conditions  of  debility  associated  with  old  age  much  caries  of  cementum 
occurs.  The  patients  are  often  either  unwilling  or  unable  to  keep 
the  cementum  cleansed. 

Repeated  examinations  of  the  mouths  of  school-children  show  a 
deplorable  amount  of  caries  which  may,  perhaps,  be  attributable  to 
several  causes,  such  as  the  induction  of  a  lessened  systemic  resistance 
due  to  confinement,  study,  etc.,  and  also  to  the  inhalation  of  vitiated 
air,  which  presumably  also  contains  acid-producing  bacteria.  More- 
over, bacteria  of  caries  may  be  directly  transmitted  by  kissing,  common 
use  of  pencils,  etc. 

Michaels,^  of  Paris,  has  observed  that  "the  saliva  of  adolescence 
contains  a  dextrinic  principle  (glycogen)  susceptible  of  fermentation 
under  the  influence  of  ptyalin  in  the  presence  of  earthy  salts.  Lactic 
acid  is  formed." 

Bodily  Condition. — It  is  a  matter  of  observation  that  such  conditions 
as  pregnancy,  typhoid  fever,  anemia,  leukemia,  diabetes,  dyspepsia, 
nervous  exhaustion,  and  debility  are  frequently  accompanied  by  or 
followed  by  a  development  of  cavities  of  decay,  but  whether  the  dis- 
eases themselves  or  a  coincident  lack  of  oral  hygiene  act  to  permit 
the  formation  of  the  gelatinous  plaques  has  not  clearly  been  made  out. 
If  oral  and  dental  prophylaxis  be  practised  during  typhoid  fever  and 
convalescence  therefrom,  the  production  of  cavities  is  much  limited, 
but  this  does  not  prove  anything.  The  same  is  true  of  pregnancy, 
which  introduces  an  exciting  cause  (the  vomitus),  and  of  glycosuria, 
which  introduces  ghicose.     Black  contends  that  periods  of  suscepti- 

'   Sialosemiology.     See  Dental  Cosmos,  1900. 


HISTORY  AND  EXCITING  CAUSES  321 

bility  are  noted  both  in  apparent  good  and  ill  health.  That  apparent 
health  may  really  not  be  true  health  is  a  matter  that  must  be 
considered. 

This  bodily  condition  is  seemingly  the  key  to  any  change  which 
can  occur  in  saliva,  or  mucus,  or  oral  phagocytosis,  to  one  of  which 
must  be  attributed  any  possible  systemic  effect  upon  caries  Ijacteria, 
which  can  aid  or  inhibit  their  growth  or  localization.  It  matters  very 
little  whether  the  bodily  condition,  is  due  to  heredity  as  a  general 
modification  of  cell  physiology,  to  age  or  some  period  of  stress,  as  the 
"change"  of  the  teeth,  puberty,  growth  during  adolescence,  business 
or  family  anxieties,  the  degenerative  tendencies  of  advancing  age,  or 
to  some  more  acute  systemic  condition,  as  typhoid  fever,  diabetes,  etc., 
except  in  so  far  as  these  conditions  may  introduce  into  the  oral  fluid 
a  substance  which  may  act  either  as  a  direct  decalcifying  agent  (an 
acid)  or  as  an  indirect  decalcifying  agent  by  furnishing  a  food  material 
for  the  bacteria  from  which  they  may  manufacture  acid. 

It  was  shown  under  the  caption  of  Erosion  that  a  very  weak  acid 
may  decalcify  more  rapidly  than  a  stronger  solution,  and  it  has  been 
noted  that  in  systemic  conditions  inducing  general  acidosis  (as  chronic 
nephritis  or  diabetes)  there  is  a  tendency  to  deep  decalcification  of 
cei-vices  of  teeth,  beginning  particularly  upon  the  cementum.  While 
by  no  means  proved  not  due  largely  to  fermentation  of  carbohydrate 
food  by  bacterial  plaques,  as  a  result  of  defective  hygiene,  there  is, 
nevertheless,  a  strong  suspicion  that  the  acidosis  expressed  as  acidity 
of  saliva  has  produced  the  decalcification.  There  is  also  a  probable 
reduction  in  the  amount  of  normal  .sodium  phosphates  as  the  result 
of  the  general  acidosis,  and  this  also  found  in  the  saliva  reduces 
the  controlling  quality,  which  Head  has  shown  to  exist  when  a  certain 
percentage  of  basic  sodium  phosphate  is  present  in  solutions  having 
an  acid  reaction.  (See  pages  88  and  284.)  On  the  other  hand,  in 
such  a  condition  as  diabetes  there  is  not  only  a  general  acidosis,  but 
also  the  possible  transudation  of  a  glycogenic  principle  into  the 
saliva  which  can  undergo  acid  fermentation  by  oral  bacteria. 

Michaels"  states  that  the  constitution  of  the  saliva  changes  with 
the  establishment  of  various  diatheses,  and  that  a  physiological 
saliva  with  the  biochemical  principles  in  a  state  of  equilibrium  is 
probably  very  rare.  He  states  that  the  most  active  dental  caries  is 
found  in  the  mouths  of  hy])o-acid  individuals,  in  whom  saline  chlorides 
predominate  over  the  acitl  elements  of  metabolic  waste,  reducing  the 

I  Dental  Cosmos,  December,  1900. 
21 


322  DENTAL  CARIES 

acidity  of  body  fluids  below  normal  and  inducing  a  lessened  resistance 
to  development  of  infective  causes,  and  least  active  in  the  hyperacid 
individuals,  in  whom  sulphocyanide  of  potassium  is  more  abundant 
in  the  saliva. 

Kirk  claims  that  "through  diathetic  fault  or  error  in  metabolism, 
the  buccal  secretions  are  charged  with  a  waste  product  which  con- 
stitutes the  most  acceptable  pabulum  for  the  development  of  caries 
producing  fungi,"  and  is  of  the  opinion  that  immunity  to  caries  is 
rather  due  to  the  absence  of  this  pabulum  than  to  any  immunizing 
principle  in  the  saliva/ 

He  has  succeeded  in  altering  viscid  saliva  to  a  more  limpid  condi- 
tion by  reducing  the  ratio  of  carbohydrate  to  proteid  diet,  first  cutting 
out  carbohydrates  almost  altogether,  then  adding  them  gradually  to 
the  diet.  He  cites  observations  upon  asylum  children  kept  upon  a 
well-balanced  ration  as  having  large  numbers  of  arrested  caries.^ 

Black'  believes  that  the  condition  of  the  system  alters  the  oral  fluid 
so  as  to  permit  the  bacteria  in  it  to  produce  a  gelatinoid  material  as  a 
by-product  in  one  case  and  not  to  produce  it  in  another,  and  that 
when  produced  plaques  adhere  to  the  teeth  in  sheltered  spots,  while 
when  not  produced  no  plaques  adhere,  though  a  general  acidity  of  the 
oral  fluids  may  be  produced. 

Miller,*  some  years  ago,  pointed  out  that  filthy  mouths  often  do  not 
contain  carious  teeth.  He  offered  the  rational  explanation  that  the 
unchanged  food  particles,  once  their  acid-producing  capacity  is 
destroyed,  can  even  act  as  a  protection  in  so  far  as  caries  is  concerned. 
The  fact  that  fairly  cared  for  mouths  often  contain  carious  teeth  is 
rather  an  argument  in  favor  of  the  local  etiology  of  caries,  as  teeth 
unbrushed  after  a  meal,  or,  rather,  not  thoroughly  cleansed,  as  is  the 
rule  in  a  vast  majority  of  mouths,  contain  every  necessary  factor  of 
caries,  including  a  renewal  of  fresh  carbohydrate  food  for  the  bacteria. 

1  Dental   Co.smos,   1904.  2  Dental  Brief,  1907. 

•■"  Dental  Digest,  1907.  "*  Lecture  at  the  University  of  Pennsylvania. 


CHAPTER    XII. 

DENTAL  CARIES:    PATHOLOGY,  MORBID  AxM ATOMY,  Ax\D 
CLINICAL  HISTORY. 

PATHOLOGY  AND   MORBID   ANATOMY. 


It  is  a  fact  of  common  observation  tliat  caries  begins  only  at 
spots  protected  from  friction  or  nncleansed.  These  are  in  order  of 
frequency:  (1)  pits,  grooves,  and  fissnres  in  the  enamel;  (2)  approximal 
surfaces  jnst  above  the  contact  point;    (3)   smooth  snrfaces  which 


Fio.  275 


Fig.  277 


Fig.  278 


Fig.  279 


Fig.  280 


Fig.  281 


Fig.  284 


Fig.  28.5 


Fig.  286 


Fig.  287 


Fig.  288 


from  any  canse  are  habitnally  unclean;  (4)  necks  of  the  teeth  at  or 
near  the  junction  of  the  cementum  and  enamel  (Black)  (Figs.  275 
to  288.) 

In  these  situations  Williams  has  demonstrated  the  fact  that  the  oral 
bacteria,  protected  from  friction,  attach  themselves  to  the  enamel, 
forming  raicrobic  plaques  which  are  sufficiently  adherent  to  permit 


324 


DENTAL  CARIES 


their  retention  during  the  grinding  of  the  specimen  for  microscopic 
examination.  (See  Figs.  289,  290,  and  291.)  Carbohydrate  food 
debris  lodges  at  the  points  at  which  retention  is  favored,  and  either 
ferments  directly  against  the  enamel  or  through  the  medium  of  the 
microbic  plaque. 

The  bacteria  in  the  plaque  require  food  and  obtain  it  from  the 
carbohydrate  and  albuminous  materials  which  come  in  contact  with 
them.     From  the  carbohydrates  lactic  acid  is  produced  as  a  waste 

Fig.  289 


Section  of  normal  human  enamel,  showing  thick,  felt-like  mass  of  microorganisms  slightly 
raised  from  the  surface  of  the  tissue  by  pressure  of  the  cover-glass  in  mounting.  X  250. 
rWilliams.) 

product.  (See  Chapter  XL)  Williams  states  that  it  is  "highly  im- 
probable that  the  enamel  is  affected,  except  in  rare  and  special 
instances  })y  any  other  acid  than  that  which  is  being  excreted  by  the 
bacteria  at  the  very  point  at  which  they  are  attached  to  the  enamel." 

This  thick  mass  of  fungi  also  prevents  the  excreted  acid  from  being 
washed  away,  so  that  it  exerts  its  full  chemical  power  upon  calcific 
tissue. 

The  lactic  acid  produced  attacks  the  inorganic  matter  of  the  enamel, 
following  first  the  interprismatic  cement  substance  between  the  prisms. 


PATHOLOGY  AND  MORBID  ANATOMY 


325 


later  dissolving  the  transverse  cement  substance  between  the  globules. 
The  effect  is  to  produce  an  irregular,  roughened  surface  of  the  enamel 
and  to  bring  into  view  the  structure  of  the  rods  (Fig.  296). 

The  gradual  loss  of  cement  substance  unbinds  the  enamel  globules, 
which  are  in  turn  dissolved  and  washed  away,  leaving  a  depression 
or  cavity. 

Fig.  290 


^ 


> 


Microoigaiiisius  of  caries  attached  to  enamel  <ui  ;ipi>rci\imal  surface  of  tooth.    (Williams.) 

In  the  process  of  enamel  dissolution  the  bacteria  may  enter  the 
crevices  formed  by  solution  of  the  interprismatic  cement  substance 
and  by  repetition  of  the  process  gain  access  to  the  dentine  (Fig.  299). 

The  form  of  the  enamel  may  be  retained  until  and  even  after 
decalcification  has  readied  the  dentine,  riinically  this  is  seen  as  a 
ch.seolored  spot,  resisting  the  instrument  until  some  force  is  used,  when 
it  rapidly  breaks  down  (Fig.  291). 


326 


DENTAL  CARIES 
Fig.  291 


Superficial   approximal   caries  of  enamel   with   films;   also   shows   slight  approximal 
abrasion.     (Miller.) 

Pig.  292 


Budding  of  spores  on  the  stems  of  leptothrix  racemosa.     (Williams.) 


PATHOLOGY  AND  MORBID  ANATOMY 


327 


A  central  cavity,  or  several  minute  openinfj^s,  leading;  to  or  almost 
to  the  dentine,  is  sometimes  seen  in  the  general  deealciHecl  area.  It 
signifies  the  loss  of  the  orijjanic  matter  of  tlie  enaiiicl  hy  uiihinding  or 
peptonizing  actions.  The  extraction  of  an  approximatino;  tooth  per- 
mits the  film  to  he  rubbed  ort'  or  prevents  the  retention  of  carbcjliydrate 
media,  so  that  the  bacteria  cease  to  be  active,  and    this  spot  may 


Fk;.  293 


Tliick  Kniwtli  iif    leptiilhrix   raceiiiosii  fnii-lilicatioii  lieails  frmn  appruxiinal   surface  i)f    Icmlli, 
under  high  magnifying  power.     (Williams.) 


remain  indefinitely  at  this  point — c.  r/.,  the  (hsease  is  arrested.  It  may 
cease  spontaneously  to  further  develop,  owing  to  the  estal)lishment 
of  an  inununizing  systemic  change,  even  though  the  teeth  remain  in 
approximation,  and  strict  pro])hylaxis  will  usually  arrest  the  advance 
of  the  process. 

It  is  also  noted  clinically  and  microscopically  that  the  decalcification 


328 


DENTAL  CARIES 

Fig.  294 


A  form  of  streptococcus  found  abundantly  in  mouths  where  very  rapid  decay  of  teeth 
is  in  progress.      X  750.     (Williams.) 

Fig.  295 


Scrapings  of  microorganisms  frnm  IIjc  apfiroxirn.il  wiir  t.utf^  of  a  decaying  tooth:   shows  the  lepto- 
thrix  buccalis  maxima  and  the  bacillus  buccalis  maximus  of  Miller.      X  1500.     (Williams.) 


PATHOLOGY  AND  MORBID  ANATOMY 


329 


is  deepest  at  a  spot  just  al)ove  the  point  of  contact,  and  less  deep  at 
points  buccal  or  lingual,  occlusal  or  cervical,  to  this  spot,  and  still  less 
at  points  more  buccal  or  lingual — i.  e.,  it  shades  off  to  zero  lingually, 
buccally,  occlusally,  and  cervically  (Fig.  300).  Bacteria  growing  in 
the  spaces  from  which  the  interprismatic  cement  substance  has  disap- 
peared cause  detachment  of  masses  of  partially  decalcified  rods 
(Figs.  299  and  301). 


Fig, 296 


i  «i 


•  t    ^ 


Section  through  human  enamel,  showing  first  stages  of  caries — i.e.,  solution  of  interprismatic 
cement  substance.     To  be  compared  with  Fig.  159.     (Williams.) 

The  dentine  may  in  .such  cases  be  deeply  affected.  When  the  entire 
thickness  of  the  enamel  is  penetrated  and  the  dentine  attacked,  there  is 
a  change  in  the  mode  of  progress  of  the  decalcification,  which  pro- 
ceeds along  the  line  of  union  between  the  enamel  and  dentine,  as 
well  as  directly  into  the  dentine  (Fig.  300);  in  this  way  the  enamel  is 
attacked  from  its  dentinal  side  (Fig.  29S)  (backward  caries). 

In  (ho  ultimate  breaking  down  of  the  enamel  the  rods  first  separate; 
the  outlines  of  the  .several  globules  of  which  the  rods  are  composed  are 
brought  into  plain  view;  next,  the  calcified  plasmic  strings  noted  in 


330 


DENTAL  CARIES 


enamel  formation  become  evident;  and  finally,  the  bead-like  masses 
upon  these  strings  are  left  as  the  ultimate  granular  detritus  of  the 
enamel. 

In  cases  of  rapid  enamel  dissolution  Williams  found  streptococci 
almost  invariably  present;  and  suggests  tentatively  that  the  variety  of 
organisms  may  be  the  factor  governing  the  rapidity  of  dissolution 
(Fig.  294). 

These  are  probably  the  Streptococcus  brevis  of  Goadby  (Micro- 
coccus nexifer  of  Miller). 

Fig.  297 


Section  of  human  bicuspid,  showing  commencement  of  caries:  a  and  a',  appearances  caused 
in  enamel  and  dentine  by  the  acid  of  decay;  b  and  b'^,  shreds  of  a  felt-like  mass  of  bacteria  raised 
from  the  surface  of  the  enamel ;  c,  a  cavity.      X  12.     (Williams.) 


Williams  found  Streptococcus  pyogenes  albus  and  aureus  and  sar- 
cinea  lutea  to  be  acid  producers. 

The  large  cocci  and  diplococci  shown  in  Fig.  301  were  always 
found  in  the  secondary  decay  of  enamel. 

"In  the  direct  caries  of  enamel  the  cavities  arc  lined  with  Icptothri.x 
and  thread-like  forms"  (Fig.  293). 

"The  leptothrix  buccalis  maxima  and  the  hacilkis  biiccalis  niaxiinus 
of  Miller  are  nearly  always  found,  the  latter  more  sparingly"  (Fig.  295). 


PATHOLOGY  AXD  MORBID  ANATOMY 


331 


Some  of  these  bacteria  are  not  acid  producers,  and  it  may  he  that 
if  a  film  is  composed  entirely  of  these  they  may  occupy  a  field  and 
really  protect  it  by  being  acidly  inactive. 


Fig.  298 


Section  of  carious  tooth,  showing  appearances  of  decay  in  enamel  and  dentine  at  the  line  of 
union  of  these  tissues;  the  dark  spots  shown  in  the  enamel  and  dentine  are  masses  of  micro- 
organisms.     X  250.      (Williams.) 

Fig.  299 


Penetration  of  bacilli  between  enamel  prisn;  -   nition  of  interprisinatic  cement 

substance.     (.Miller.) 

"Beneath  the  felt-like  masses  of  thread  forms  and  lying  in  contact 
with  the  decomposing  enamel  in  direct  decay,  and  also  in  deep  cracks 


332 


DENTAL  CARIES 


and  fissures  in  secondary  decay,  there  is  invariably  found  a  short, 
thick  bacilhis,  usually  constricted  in  the  centre"  (Williams,  also 
Goadby). 

Caries  of  Nasmyth's  Membrane. — Miller^  demonstrated  that  the 
enamel  cuticle  may  act  as  a  breeding  ground  for  many  forms  of  bacteria 
which  occupy  it,  forming  a  matrix  which  may  retain  minute  particles 
of  food,  which  in  turn  aid  in  acceleration  of  the  progress  of  decay 
(Fig.  304). 

Fig.  300 


Decalcification  of  enamel  without  loss  of  form:  a,  film.      X   35.      (Miller.) 

Caries  of  Dentine. — The  bacteria  after  penetrating  the  su Instance 
of  the  enamel  attack  the  dentine.  This  presents  a  different  anatomical 
and  chemical  structure  to  be  acted  upon.  Beneath  the  enamel  the 
first  layer  of  dentine  is  of  a  composition  which  permits  the  bacteria 
to  rapidly  .spread  laterally  along  this  zone.  They  also  enter  the  tubules 
of  tlie  dentine  and  penetrate  })y  multiplication  toward  tlie  pulp.  A 
wedge-shaped  area  of  decay  is  prochiced  (Figs.  300  and  300). 

In  all  ca.ses  decalcification  precedes  these  invasions.  At  the 
periphery  the  tul^ules  communicate  freely  by  their  lateral  branches 

'  Microorganisms  of  the  Human  Mouth,  1890,  and  Dental  Cosmos,  1900. 


PATHOLOGY  AND  MORBID  ANATOMY 


333 


(Fig.  305),  and  the  lateral  spreading  of  the  l)actoria  by  multiplication 
is  readily  explained. 

It  is  seen  clinically  in  caries  that  a  portion  of  the  dentine  is  abso- 
lutely destroyed  and  removed,  leaving  within  the  tooth  a  "cavity  of 
decay"  l)ounded  by  dentine  and  enamel  undergoing  disintegration; 


Fig.  301 


Cover-glass  preparation  from  scrapings  of  white,  opaque,  decaying  enamel:  the  cement  sub- 
stance between  the  rods  is  seen  to  be  dissolved  away,  and  the  crevasses  thus  formed  are  filled 
■with  round  and  oval  forms  of  micrococci  and  bacteria.  Stained  by  the  Gram  method.  X  450. 
(Williams.) 

beneath  this  lies  dentine  less  affected,  and  beneath  this,  .sound  dentine 
(Fig.  30())-     These  phenomena  require  explanation. 

The  tubules  of  the  decalcified  dentine  become  packed  for  a  distance 
with  bacteria  (Figs.  307  and  300).  'iliese  act  upon  tiie  organic 
matrix  of  the  decalcified  tubule  walls.  The  internal  {)ressure  due  to 
multiplication  distends  them  so  that  the  lumen  is  enlarged.  At  the 
same  time  the  bacteria  excrete  a  ferment  or  ferments  which  cause  the 
wall   at  first   to   thicken.     The   dilatation   and   thickening   together 


334 


DENTAL  CARIES 


cause  the  compression  of  the  decalcified  intertubular  substance,  and 
the  tubules  assume  an  hexagonal  shape  owing  to  the  mutual  pressure. 


Various  forms  of  micrococci  and  bacteria  from  decaying  enamel.     Photographed  by  Mr.  Andrew 
Pringle  from  Williams'  cover-glass  preparation.      X  1000.     (Williams.) 

Fig.  303 


Cover-glas.H  preparatif)ns  of  scraiiings  from  dcciy  of  enamel:  shows  leptothrix  buccalis  maxima 
and  bacillus  huccalis  maximu.4  of  Miller.     Stained  by  Gram  method.      X  830.     (Williams.) 


PATHOLOGY  AND  MORBID  ANATOMY 


335 


The  phenomenon  is  not  a  vital  one,  as  it  occurs  in  artificial  caries 
(Miller)  (Fig.  30S). 

Fig.  304 


Enamel  cuticle  permeated  by  bacteria.      (1100  to  1.)      (Miller.) 

The  bacterial  ferment  possesses  a  digestive  or  peptonizing  power 
analogous  to  trypsin  and  begins  to  liquefy  the  inner  surface  of  the 
tubule  wall.     As  it  does  so  the  lumen  is  further  increased  and  the 

Fig.  .305 


Carious  dentine,  stained  with  fuclisin  to  show  microorganisms.  The  section  shows  the  con- 
dition of  the  tubules  as  filled  with  microorganisms  along  the  junction  of  the  dentine  with  the 
enamel  at  a.     The  tubules  are  very  much  enlarged,      ('/lo  immersion  oljjective.)      (Black.) 

bacteria   fill    the  acquired   space.     Taking  up   carbohydrates  lactic 
acid  is  produced,  which  combines  with  the  calcium  salts  of  deeper 


336 


DENTAL  CARIES 


tubules  and  intertubular  substance  and  prepares  a  path  of  decalci- 
fied tissue  for  bacterial  advance  (Fig.  309). 


Fig.  306 


Longitudinal  ground-section  through  the  crown  of  an  inferior  niolar  of  a  negro:  E,  enamel; 
D,  dentine;  C,  cement;  p,  pulp  cliamber;  a,  large  decay,  from  the  occlusal  surface;  b,  small 
decay,  from  the  niesal  surface;  cs,  cone  of  sepfic  invasion  and  discoloration;  e,  partially  decal- 
cified and  discolored  enamel  around  the  carious  cavity;  z,  dark  cones;  2',  clearer  cones;  z^p, 
oldest  cones  where  putrefaction  of  the  tooth  cartilage  begins;  c,  outer  transparent  zone,  or  zone 
of  Tomes;  sd,  secondary  dentine,  caused  by  irritation;  s^d^,  secondary  dentine  deposited  by 
normal  physiological  process,  recession  of  the  pulp.  This  figure  is  drawn  from  a  ground  and 
polished  .section  mounted  in  Canada  balsam.     (Gysi.) 

This  combination  of  the  acid  with  the  calcium  salts  disposes  of  or 
neutralizes  the  acid,  which,  if  accumulated  to  the  strength  of  2  per 


PATHOLOGY  AND  MORBID  ANATOMY 


337 


cent.,  would  ciuisc  the  (Icstrtictioii  of  the  bacteria  (by  their  waste 
pro(hicts).  (MiUer.)  Calcium  lactophosphate,  calcium  lactate,  and 
magnesium  lactophosphate  are  produced. 


Fig.  307 


Carious  dentine,  showing  invaded  tubules 
and  uninvaded  but  decalcified  intertubular 
substance.      (Miller.) 


Fia.  308 


'^f. 


^ 


Cross-section  of  decayed  dentine:  the  tubules 
through  reciprocal  pressure  have  assumed  the 
shape  of  5-  and  6-sided  prisms.     (Miller.) 


Miller  experimentally  found  that  the  calcium  carbonate  does  so 
neutralize  the  acid  formed  by  formation  of  calcium  lactate,  but  the 
calcium  phosphate  does  not,  as  it  develops  calcium  lactophosphate, 


Fig.  309 


Section  of  decalcifioci  dentine  partly-  invaded  by  bacteria:  o,  uninvaded  zone.     (Miller.) 

setting  free  })hosj)horic  acid,  which    maintains  the  relative  acidity. 
Experimentally  the  addition  of  calcium  phosphate  to  a  solution  of 
22 


338 


DENTAL  CARIES 


lactic  acid  did  not  reduce  the  decalcification  in  pieces  of  dentine  placed 
in  it,  for  the  reason  named. 

The  bacterial  ferments  continue  to  digest  the  wall  of  the  tubule, 
and  a  time  arrives  when  they  have  penetrated  its  substance.     The 


Fig.  310 

lite,, 


Fig.  311 


Ml 


M  I 


Liquefaction  foci.     (Miller.) 


I 


Decayed  dentine  showing  a 
mixed  infection  with  cocci  and 
bacilli.      X  400.      (Miller.) 


intertubular  substance  is  then  removed  in 
like  manner.  The  same  process  occurring 
in  adjoining  tubules  as  well,  the  entire 
dentinal  substance  in  the  particular  area 
at  the  cavity  surface  is  destroyed — i.  e., 
liquefied  and  washed  away  (Fig.  306,  a). 

Occurring  at  a  point  beneath  the  general 
cavity  surface,  the  bacteria  in  several  adjoining  tubules  destroy  their 
walls  and  the  intervening  intertubular  substance,  forming  what 
Miller  has  called  a  "liquefaction  focus"  (pi.  foci)  (Fig.  310).  This 
action  proceeds  until  the  enamel  is  undermined  and  the  pulp  is  ex- 
posed. A  decalcified  area  always  exists  in  advance  of  the  tubule 
invasion,  sometimes  large  masses  being  found,  though  it  lessens  in 
quantity  as  th(>  pulj)  is  approached. 

As  the  enamel  is  undermined  by  the  carious  process  the  bacteria 
and  their  acids  decalcify  its  inner  surface,  the  process  proceeding 
from  within  outwaid  and  termed  "secondary  caries,"  or  "backward 
caries,"  of  enamel. 

The  enamel  is  thus  weakened  and  at  the  same  time  deprived  of 
dentinal  support,  and  breaks  down  under  stress  of  mastication. 


PATHOLOGY  AND  MORBID  ANATOMY 


339 


Any  interglobular  spaces  in  the  dentine  being  filled  with  transi- 
tional or  uncalcified  material  like  the  tubule  walls  are  rapidly  invaded 
by  the  bacteria  during  their  progress  along  the  tubules  (Fig.  312). 

The  character  of  the  organisms  in  the  tubules  and  the  nature  of 
the  liquefaction  seem  to  depend  upon  the  particular  germs  present. 


Fig.  312 


Interglobular  spaces  filled  with  bacteria. 


(Miller.) 


INIiller  has  shown  that  in  the  deeper  portions  of  tubules  micrococci 
appear  to  predominate  over  the  rod  forms,  which  are  also  present; 
although  one  tubule  may  be  filled  with  cocci  and  its  neighbor  with 
rod  forms  (Fig.  311).  It  is  only  in  the  more  superficial  layers  that 
the  thread  forms  are  found  in  numbers. 

Goadby^  has  done  much  interesting  work  in  tliis  direction,  and 
offers  the  following  classification  of  bacteria  found  in  decayed  dentine: 

Bacteria  of  Dental  Caries. 
Acid-forming  Bacteria. 

•       ■       •       1 
■      ■      ■       ) 


Streptococcus  brevis    . 
B.  necrodentalis 
Staphylococcus  albus 
Streptococcus  brevis    . 
Sarcina  lutea    . 
Sarcina  aurantiaca 
Sarcina  alba  (Eisenberg) 
Staphylococcus  albus 
Staphylococcus  aureus 


Deep  layers  of  carious  dentine. 


Superficial  layers  of  carious  dentine. 


Bacteria  which  Liqueju  Dentine  (Decalcified). 

None  i.solated  as  yet Deep  layers  of  carious  dentine. 

B.  mesentericus  ruber 
B.  mesentericus  vulgatus 
B.  mesentericus  fuscus 

B.  fervus 

B.  gingivae  pyogenes    .... 
B.  liquefacieiis  fluore-scens  motilis 

B.  subtilis 

Proteus  Zeiikcri 

B.  plexiformis 


Superficial  layers  of  carious  dentine. 


Mycology  of  the  Mouth,  and  Dental  Cosmos. 


340  DENTAL  CARIES 

Goadby  states  that  his  experiments  show  that  the  bacteria  which 
dissolve  blood  serum  also  digest  decalcified  dentine,  while  those  which 
only  liquefy  gelatin  do  not  digest  decalcified  dentine. 

His  experiments  also  indicate  that  of  the  bacteria  found  in  the 
superficial  layers  of  carious  dentine  some  produce  digestive  enzymes, 
others  acid  fermentation,  and  others  have  both  functions. 

Choquet^  has  confirmed  the  observation  of  Miller,  Vignal,  Gallipe, 
and  Goadby,  that  the  deeper  the  portions  of  dentine  examined  the 
fewer  species  of  fungi  are  found  in  the  tubules,  and  explains  it  upon 
the  ground  that  the  anaerobic  or  facultative  aerobic  organisms  in  the 
outer  layers  advance  into  the  deeper  dentine  because  they  are  better 
suited  to  the  conditions. 

These  exact  findings  are  interesting  as  bearing  out  the  general 
demonstrations  of  Miller;  at  the  same  time,  Miller's  experiment  show- 
ing absolute  dissolution  by  a  single  bacterium  in  pure  culture  is  to  be 
recalled. 

Choquet^  has  shown  that  dental  caries  may  proceed  under  fillings 
against  sound  dentine  by  the  following  experiment: 

Artificial  cavities  were  prepared  in  the  incisors  of  a  sheep.  In  these 
was  securely  sealed  with  cement  a  small  particle  of  a  gelatin  culture 
of  caries  fungi  applied  on  a  sterilized  platinum  cap.  Nine  months 
later  the  dentine  had  become  yellow,  slightly  decalcified,  and  the 
tubules  penetrated  by  bacteria.  Tliis  softened  dentine  was  used  to 
inoculate  a  portion  of  the  medium  originally  used,  and  the  species 
again  cultivated. 

Miller^  estimated  the  relative  loss  of  inorganic  and  organic  matter 
in  dentine  during  the  process  of  caries  by  weighing  and  analyzing 
equal  volumes  of  carious  and  sound  dentine  from  the  same  teeth. 

The  carious  dentine  had  lost  about  seven-ninths  of  its  weight, 
which  was  due  to  the  loss  of  twelve-thirteenths  of  its  original  calcium 
salts  by  decalcification,  and  two-fifths  of  its  original  organic  matter 
by  liquefaction  of  its  substance. 

Tube  Casts. — In  the  zone  of  decalcification  in  advance  of  bacterial 
invasion  of  the  tubes  are  foimd  rod-shaped  bodies  or  shining  granules, 
first  described  by  J,  Tomes.  They  occur  in  botli  natural  and  artificial 
caries,  hence  it  must  be  inferred  that  their  presence  is  not  the  result 
of  a  vital  process. 

The  rods  do  not  dissolve  in  organic  acids,  but  dilute  sulphuric  acid 

'  Microbes  of  Dental  Caries,  Dental  Cosmos,  1900.  ^  Ibid. 

*  MicroSrganisms  of  the  Human  Mouth. 


PATHOLOGY  AND  MORBID  ANATOMY  341 

quickly  dissolves  them.     They  are  unaffected  by  alcohol  or  chloroform, 

a  proof  that  they  are  not  composed  of  fat.     Miller  regards  them  as 

probably  calcic  formations  against  the  tubule  wall  as  a  cast  of  the  wall, 

and  which  become  loosened   when  enlargement  of 

the  tubule  occurs.     They  have  a  tubular  structure,  ^"'-  ^'^ 

are  brittle,  and  may   contain   a    central   thread-like 

filament  which   may  possibly  be  the  remains  of  a 

dentinal  fibril.     Bacteria   may  surround   them,  but 

do    not    enter    them.      The   granules   are   probably 

broken  rods.^     The  data  point  toward  a  probability 

that  the  rods  are  composed  of  calcium  lactate  and 

calcium  lactophosphate,  the  result  of  a  combination 

of  the  lactic  acid  with  the  calcium  salts  of  the  dentine.        x„be  casts. 

The  resultant  salt   is  probably  deposited  as  a  tube 

cast,  as  suggested  by  Miller.     Polariscopic  experiments  should  be 

competent  to  settle  the  question. 

The  Transparent  Zone. — Around  the  zone  of  decalcified  uninfected 
dentine  appears  a  zone  of  dentine  more  transparent  than  the  surround- 
ing normal  dentine.  The  zone  extends  from  periphery  to  periphery 
around  the  cone  of  carious  dentine  (Fig.  306,  c).  The  tubules  in  this 
area  contain  granular  matter  not  seen  in  normal  dentine  nor  in  the 
dentine  of  dead  teeth  in  the  same  situation.^ 

Tomes  and  iMagitot  both  regarded  the  transparency  as  an  attempt 
made  by  nature  to  impede  the  progress  of  caries.  Walkhoff  regards 
it  as  due  to  a  sclerotic  action,  the  fibrilla?  upon  stimulation  producing 
intercellular  substance  (tubule  wall)  at  their  own  expense  and  prima- 
rily of  their  offshoots.  Black  once  regarded  it  as  the  earliest  stage 
of  decalcification,  but  has  discarded  this  idea.  Miller  advanced  the 
following  data  :^ 

1.  Transparency  indicates  increased  homogeneity  as  opposed  to  the 
heterogeneity  of  normal  dentine — i.  e.,  the  co-efficients  of  light  refrac- 
tion are  brouglit  nearer  together. 

2.  It  occurs  in  living  dentine  only  and  is  not  found  in  natural  teeth 
mounted  on  plates  and  decayed  in  the  mouth,  nor  in  secondary  caries 
of  denthie  from  the  pulp  cavity  to  the  peripiiery,  and  is,  therefore,  a 
result  of  vital  action.  (Compare  Figs.  300  and  316  with  Figs.  314 
and  315.) 

3.  The  tubules  have  their  lumen  lessened  in  diameter  in  the  trans- 
parent areas,  an  agreement  with  the  position  of  Walkhoff. 

'  Miller.  '  Ibid.  *  Microorganisms  of  the  Human  Mouth. 


342 


DENTAL  CARIES 


4.  Secondary  dentine  may  accompany  the  process  in  contiguity 
with  the  area;  moreover,  secondary  dentine  is  transhicent.  It  indicates 
a  constructive  excitation  of  the  odontoblasts,  of  which  the  dentinal 
fibrils  are  prolongations  (Fig.  308,  Sd). 

5.  Chemical  analysis  proved  that  no  lime  salts  had  been  lost,  and 
it  was  pointed  out  that  a  gain  in  the  percentage  of  salts  was  unnecessary, 
as  new  dentine  is  necessarily  composed  of  organic  as  well  as  inorganic 
matter,  wherefore  the  analysis  would  not  necessarily  vary  from  that 
of  normal  dentine. 

Fig.  314 


Section  from  a  lower  incisor  worn  on  a  plate:  extensive  decay  without  increase  of 
transparency.      X  15.     (Miller.) 

6.  It  is  found  in  connection  with  abrasion  of  human  teeth  in  which 
the  activity  of  acid  may  possibly  be  an  open  question,  and  it  also 
occurs  in  the  worn  teeth  of  dogs,  the  saliva  of  which  is  strongly  alkaline. 

Miller  states  that  opacity  may  follow  or  be  associated  with  trans- 
parency.^ 

The  natural  conclusion  is  that  the  transparency  is  a  form  of  tubular 
calcification,  and  that  it  impedes  the  progress  of  caries;  that  it  does 
not  succeed,  as  a  rule,  is  due  to  the  overwhelming  action  of  the  bacteria. 

In  cavities  from  which  the  walls  are  broken  away,  freely  exposing 

>  Dental  Cosmos,  April,  1903. 


PATHOLOGY  AND  MORBID  ANATOMY 


343 


the  carious  dentine  to  mastication,  the  carious  dentine  and  its  con- 
tained l)acteria  may  be  removed  by  friction  (Fig.  .324). 

In  the  transparent  area  the  tubules  become  obliterated;  a  polished, 
discolored  surface  results  resembling  in  degree  an  abraded  surface. 
This  process  is  called  "eburnation,"  and  is  really  tubular  calcification 
(which  see).  In  the  same  tooth  a  more  sheltered  border  of  this  spot 
may  be  undergoing  the  carious  process.  Miller  records  cases  of  l^adly 
decayed  teeth  in  which  the  process  ceased  spontaneously  and  the  den- 
tine became  hard  and  smooth. 


Secondary  caries  of  dentine  advancing  from  i)ulp  chamber  and  therefore  occurring  after 
death  of  the  pulp.     Absence  of  transparency.      X  15.     (Miller.) 

Pigmentation  in  Caries. — Pigmentation  occurs  in  caries  possibly  from 
extraneous  sul)stances  entering  the  carious  area,  po.ssibly  from  the 
substances  formed  during  putrefaction. 

The  slower  the  progress  of  the  decay  the  greater  the  discoloration. 
The  colors  vary  from  light  yellow  to  reddish  brown,  dark  brown, 
and  black. 

The  color  is,  as  a  rule,  darkest  u])()n  the  outside  of  the  carious 
dentine,  but  the  pigment  may  extend  through  large  masses  and  be 
found  staining  dentine  l)eneath  the  caries  hard  enough  to  leave 
ill  situ.     As  a  rule,  this  is  not  the  case. 


344 


DENTAL  CARIES 


Black  suggests  the  possible  formation  of  sulphides.  Miller  has 
found  iron  almost  constantly  present  in  carious  dentine.  The  dis- 
coloration of  dentine  does  not  seem  to  be  necessarily  due  to  the  carious 
process,  as  it  may  be  seen  in  areas  of  abrasion.  In  a  specimen  pos- 
sessed by  the  editor  a  limited  cervical  caries  caused  a  growth  of 
secondary  dentine  and  an  area  of  tubular  calcification.  From  the 
pulpal  surface  of  the  secondary  dentine  to  the  area  of  caries  extends 
a  sharply  defined  area  which  has  a  flesh-iose  color  (Fig.  317).  Many 
areas  of  secondary  dentine  due  to  abrasion  are  stained  a  dark  brown. 


Fig.  316 


Transparency  resulting  from  cracks  in  the  enamel  at  a  and  6.      X  20.      (Miller.) 

Artificial  caries  produced  in  teeth  placed  in  a  mixture  of  bread 
and  saliva  and  the  mixture  constantly  renewed  was  white.  If  putre- 
faction was  allowed  to  occur,  discolorations  ensued  (Miller). 

The  discolorations  of  carious  dentine  may  be  due  to  the  action  of 
chromogenic  bacteria.  Miller  isolated  from  the  mouth  an  organism 
which  he  named  bacillus  fuscans,  and  "which,  cultivated  on  the 
surface  of  nutritive  agar-agar,  in  a  few  weeks  imparts  to  the  medium 
a  yellowish  l)rown  color,  which  gradually  darkens  and  extends  deeper 
into  the  sul)stratiim  as  the  age  of  the  culture  increases." 

It  is  significant  that  tlie  three  acid-forming  organisms  found  by 


CLINICAL  HISTORY  OF  CARIES  345 

Goadby  in  the  deep  layers  of  carious  dentine  do  not  form  pigment 
in  their  artificial  media. 

Caries  of  Cementum. — Caries  of  cementum  occurs  when  the  gum 
has  receded,  exposing  the  cementum  to  the  fluids  of  the  mouth.  As 
a  rule,  a  triangular  depression  exists  bounded  by  the  thickened  gum 
margin,  the  cementum,  and  the  enamel.  This  favors  the  collection 
of  the  bacterial  plaques,  and  caries  follows.     The  gum  may  be  much 

Fig.  317  Fig.  318 


Cervical  caries  associated  with  secondary  Caries  of  cementum  and  dentine  com- 

dentine.     Area  pigmented.  pletely  encircling  tlie  tooth. 

receded,  yet  no  caries  occur.  As  a  rule,  however,  recession  and  un- 
cleanliness  frequently  assure  its  presence.  Especially  is  this  true 
in  cases  of  general  recession  in  aged  or  debilitated  per-sons. 

The  path  of  bacterial  invasion  after  decalcification  is  by  way  of 
Sharpey's  fibers  to  the  lacunse  and  canaliculi;  later  the  dentine  is 
invaded  as  in  the  crown.  Frequently  the  form  of  the  cementum  is 
largely  retained,  while  the  decalcification  is  deep. 


CLINICAL  HISTORY  OF  CARIES. 

The  clinical  history  of  dental  caries  records  the  observable  phe- 
nomena associated  with  its  inception,  progress,  and  termination. 

Inception  of  Caries. — Caries  begins,  after  the  manner  described  in 
the  pathology,  at  favoring  spots.  As  a  rule,  the  occlusal  fi.ssures  of 
the  molar  teeth  are  first  decayed,  the  first  molars  being  often  carious 
in  this  situation  before  fully  erupted.  Uninformed  parents  usually 
consider  this  tooth  a  temporary  one,  and  frequently  neglect  it.  It, 
moreover,  has  often  seriously  defective  fissures  which  aft'ord  lodgement 
for  gelatinous  plaques,  which  seem  to  be  readily  formed  because  of 
the  unhygienic  state  of  the  temporary  teeth,  which  are  frecjuently 
carious.     Not  infrequently  a  cavity  is  produced  on  the  mesial  surface 


346 


DENTAL  CARIES 

Fig.  319 


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Description  op  Charts. 
These  eliartu  iej>ieserit  the  number  of  carious  cavities  observed  in  one  hundred  persons,  and  the 
position  of  these  cavities  on  tlie  individual  surfaces  of  the  teeth.  There  are  five  columns  of 
.squares  devoted  to  eacli  tooth  of  one  side  of  tlie  mouth,  representing  the  five  surfaces  as  shown 
on  the  left  hand.  The  number  of  cavities  in  the  surface  represented  is  shown  by  the  number 
of  squares  darkened,  so  that  the  effect  of  the  diagram  as  a  whole  gives  a  striking  picture  of  the 
frequency  of  decay  in  the  individual  surfaces  of  the  several  teeth.  On  the  right  the  percentage, 
or  the  number  per  hundred  persons,  is  given  in  figures  calculated  to  the  first  decimal  point. 
On  the  left  the  percentage  of  cavities  in  the  individual  teeth  for  all  surfaces  is  given  in  the  same 


CLINICAL  HISTORY  OF  CARIES 


347 


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way.  Tlie  cavities  occurring  on  one  side  of  the  mouth  only  are  represented.  And  only  one 
decay  in  an  individual  .surface  is  counted;  that  is,  if  two  or  more  pits  are  found  decayed  in  the 
grinding  surface  of  a  mohir,  but  one  is  counted;  and  the  .same  rule  is  followeil  with  all  of  the 
surfaces. 

Charts  Nos.  1  and  2  (uijper  and  lower  jaw)  are  made  up  from  my  records  of  fillings  for  628 
persons  of  all  ages,  and,  therefore,  represent  what  is  seen  in  practice  rather  than  the  actual 
number  that  may  occur. 

Charts  Nos.  3  and  4  (upper  and  lower  jaw)  are  made  from  100  of  my  own  patients  between  the 
ages  of  ten  and  twenty-five  years,  for  whom  I  have  filled  all  cavities  and  know  the  condition 
at  present.  They  represent  the  actual  number  of  cases  in  which  the  individual  surfaces  have 
decayed  in  tliese  100  persons.     (Black.) 


348 


DENTAL  CARIES 


Ftg.  321 


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of  this  tooth  by  a  carious  condition  of  the  (Hstal  surface  of  the  second 
temporary  mohir.  In  other  mouths  both  teeth  are  affected  ahke,  owing 
to  the  nature  of  the  approximation.  The  relative  liabihty  of  the 
various  surfaces  of  the  (]ifferent  teetli  to  caries  may  l)e  averaged  for 
a  great  number  of  persons,  but  tables  drawn  from  ch'nical  cases  may 


CLINICAL  HISTORY  OF  CARIES 


349 


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have  little  iipplieation  to  one  partieular  iiidividiial,  a.s  peeiiliarities  of 
local  predisposing  causes  and  personal  hahits  modify  the  inception. 
Nevertheless  such  tables  are  exceedingly  interesting  as  showing  a 
general  relative  liability. 

Charts  have  been  made  by  Black  which  explain  themselves  (Figs. 


350 


DENTAL  CARIES 


319  to  322).  The  figures  given  for  the  buccal  surfaces  of  the  third 
molars  seem  rather  lower  than  those  I  would  feel  warranted  in  giving; 
certainly  after  adult  age  caries  frequently  occurs. 

The  lower  anterior  teeth  are  the  last  of  all  to  be  affected,  and  it  is 
common  to  see  the  six  lower  anterior  teeth  free  from  caries  years  after 
all  of  the  other  teeth  have  been  lost.  This  is  attributable  to  the  con- 
stant motion  of  the  saliva,  the  presence  of  calculus,  and  to  the  mechan- 
ical effects  of  tongue  movement,  lip  movement,  and  mastication. 

Fig.  323 


Caries  undermining  enamel:  o,  masses  of  bacteria  lining  the  cavity.      X  50.     (Miller.) 

In  the  t('nij)()rary  set  the  molars  decay  much  more  frequently  than 
the  incisor  teeth,  jnirtly  because  longer  retained  and  partly  because 
of  the  width  of  their  approximations.  The  pulp  is  readily  exposed 
because  of  its  relatively  larger  size. 

Approximal  cavities  are  frequently  more  broad  than  deep,  and 
present  problems  of  anchorage. 

The  Progress  of  Caries. — ^l^he  rapidity  of  progress  of  caries  depends 
upon  the  intensity  of  the  action  of  the  exciting  cause,  the  structure  of 
the  tooth,  and  the  nature  of  the  vital  resistance  offered.     The  exciting 


CLINICAL  HISTORY  OF  CARIES  351 

cause  will  act  most  intensely  in  mouths  ill  cared  for  and  containing 
much  carbohydrate  debris,  and  these  conditions  being  eqtuil,  enamel 
of  poorer  organization  and  presenting  a  greater  degree  of  solubility, 
in  teeth  presenting  broad  approximations,  will  be  the  more  rapidly 
destroyed. 

Williams  has  expressed  the  opinion  that,  as  a  rule,  the  process  of 
enamel  destruction  occupies  a  considerable  period  of  time,  a  fact 
which  may  account  for  the  general  lack  of  caries  in  the  temporary 
teeth  until  about  four  or  five  years  of  age.  The  decalcified  enamel 
may  retain  its  form  for  a  time  after  dentine  decalcification  has  begun. 
An  opaque  spot,  often  discolored,  is  seen  upon  the  tooth,  and  is  readily 
broken  down  by  an  instrument  before  dentine  decalcification  occurs. 
If  the  approximating  tooth  be  extracted  the  carious  process  may  cease, 
owing  to  the  removal  of  the  bacterial  plaque 
or  a  lack  of  food  supply  (retention).     This  ^"'f^-  ^24 

result  may  not  follow  if  the  dentine  has  been 
invaded  before  the  extraction. 

After  enamel  destruction  at  a  limited  area, 
caries  progresses  along  its  inner  side  and 
penetrates  the  dentine.  The  enamel  is  under- 
mined. The  extent  of  cavity  orifice  is  no 
certain  guide  as  to  the  depth  of  penetration. 

Cases  are  frequently  observed  in  which  the  only  external  evidence 
of  caries,  in  a  molar  or  bicuspid,  is  a  white  or  bluish  black  line  marking 
the  fissure,  and  yet  the  dentine  may  be  deeply  and  widelv  penetrated 
(Fig.  324,  A). 

As  a  rule,  however,  as  the  cavity  in  the  dentine  enlarges  the  enamel 
at  the  orifice  becomes  disintegrated,  so  that  the  orifice  is  enlarged  and 
more  food  debris  enters  to  accelerate  the  process  (Fig.  306).  A  deep 
cavity  may  thus  be  formed  before  the  patient  is  objectively  or  even 
subjectively  aware  of  its  existence.  After  a  time  the  occlusal  enamel 
boundary  of  the  cavity  breaks  down  and  food  is  even  more  readily 
admitted. 

It  has  been  noted  that  if  the  enamel  break  away  in  such  a  manner 
as  to  expose  the  carious  dentine  to  the  friction  of  food  masses  which 
are  not  retained  and  to  the  access  of  saliva,  the  progress  of  the  caries  is 
delayed  and  in  some  cases  ceases  altogether.  The  process  of  eburna- 
tion  is  set  up.  (See  Transparent  Zone  and  Tui)ular  Calcification.) 
(Fig.  324,  B.) 

Caries  may  progress  rapidly  for  a  period,  and  then  receive  a  check 


352  DENTAL  CARIES 

to  its  progress.  Teeth  previously  free  from  the  disease  may  suddenly 
fall  victims  to  its  rapid  and  widespread  progress.  No  doubt,  in  many  of 
these  cases  there  are  removed  from  or  added  to  the  local  oral  conditions 
constitutional  influences  which  deter  or  favor  the  local  development  of 
caries  producing  bacteria. 

Secondary  dentine  is  less  readily  decalcified  than  primary  dentine. 
The  process  is  sometimes  seen  in  certain  cases  in  which  caries  has  fol- 
lowed the  interzonal  or  first-formed  layer  of  coronal  dentine,  the  enamel 
chipping  off  as  undermined,  so  that  almost  the  entire  dentine  may  be 
subjected  to  this  process  and  remain  of  original  form  and  discolored 
and  eburnated.  This  is  "spreading  caries."  In  other  cases  the  tubules 
are  followed  and  the  pulp  is  rapidly  approached.  This  is  "penetrating 
caries." 

The  presence  of  great  masses  of  food  material  left  indefinitely  about 
cervices  and  without  caries  is  probably  explained  upon  the  score  of 
putrefactive  decomposition  with  protective  action. 

The  dentine  of  pulpless  teeth  is  more  rapidly  invaded  after  enamel 
decalcification  than  that  of  vital  teeth,  owing  to  the  absence  of  vital 
resistance.  This  condition  does  not  necessarily  apply  to  the  enamel 
of  pulpless  teeth. 

^\Tiile  caries  appears  at  all  ages  from  childhood  to  old  age,  its 
ravages  are  most  pronounced  and  its  progress  most  rapid  during  the 
period  of  adolescence  and  early  maturity.  Its  effects  are  most  marked 
between  the  ages  of  eight  and  twenty-five  years.  As  a  rule,  a  denture 
which  remains  at  twenty-five  years  unaffected  by  caries  remains 
unaffected  or  but  slightly  affected  to  an  indefinite  age.  To  be  sure, 
this  implies  two  conditions :  first,  that  the  active  causes  of  caries  have 
been  in  but  slight  evidence;  and  secondly,  that  the  denture  is  of  the 
highest  order.  The  classes  of  dentures  which  escape  are  perfectly 
formed  and  symmetrically  arranged  teeth,  in  the  mouths  of  patients 
who  lead  sanitary  lives  and  care  for  the  teeth,  who  masticate  vigor- 
ously, and  who  escape  other  diseases.    Very  filthy  dentures  may  escape. 

Caries  beginning  at  the  junction  of  the  cementum  and  enamel  of 
the  teeth  has  a  somewhat  different  clinical  history  from  that  noted 
when  its  occurrence  is  in  other  situations.  Its  progress  is  subject  to 
great  variations.  In  any  of  the  catarrhal  conditions  or  atroj)hic  con- 
ditions of  the  glim  which  lay  l)are  the  neck  cementum,  caries  usually 
occurs.  It  occurs  also  as  a  process  secondary  to  labial  abrasion 
and  erosion  of  the  teeth.  Teeth  affected  by  erosion,  however,  as  has 
been  pointed  out,  are  commonly  exempt  from  dental  caries. 


CLINICAL  HISTORY  OF  CARIES  353 

The  Terminations  of  Caries. — After  the  pulp  is  exposed  it  sooner 
or  later  l)ecomes  InHained  and  hypertrophies  or  dies.  In  the  latter 
case  putrefaction  results,  which  for  a  time  may  exert  a  restraining 
influence  upon  decay,  but  not  for  a  long  time. 

Masses  of  food  freely  enter  the  pulp  cavity  and  caries  proceeds  in 
the  dentine  from  within  toward  the  periphery.  This  is  "secondary 
caries"  of  dentine,  and,  occurring  in  dentine  without  vitality,  no  trans- 
parency results  (Fig.  315).  Notwithstanding,  caries  at  this  stage  pro- 
ceeds rather  slowly,  particularly  if  the  crown  he  much  broken  down. 
The  result  of  secondary  caries  is  a  hollowing  out  of  the  dentine  of  the 
root,  and  finally  a  decalcification  of  the  cementum,  which  may  persist 
for  some  time  as  a  thin,  elastic  wall.  Finally  this  is  destroyed  either 
at  the  occlusal  periphery  or  caries  causes  penetration  to  the  peri- 
cemental tissue.  This  may  occur  laterally  or  through  to  the  bifurcation 
of  the  roots.  In  either  case  it  is  called  "perforation  by  caries."  Into 
this  perforation  the  pericemental  tissue  may  become  protruded  by 
hypertrophy,  and  the  condition  of  hyperplastic  or  fungous  gum  be 
established.  Following  the  breaking  down  of  the  crown,  the  blood 
pressure  in  the  pericementum  begins  an  extrusive  process,  the  peri- 
cementum becomes  thickened,  and  the  tooth  is  somewhat  loosened. 

Decay  of  the  root  face  and  interior  and  breakage  of  the  cemental 
margins  proceed  simultaneously  with  the  extrusion  until  finally  but  a 
small  discolored  bit  of  the  root  end  lies  upon  the  surface  of  the  gum, 
from  which  it  is  removed  by  some  slight  force  or  is  extracted. 

The  entire  process  of  caries  in  a  tooth  may  thus  extend  over  a 
period  of  from  ten  to  twenty  years. 

At  times  the  extrusive  force  pushes  a  root  up  sidewise,  particularly 
when  the  tooth  has  been  tipped  over  before  the  loss  of  the  crown. 
It  may  thus  be  retained  in  position  and  attached  upon  its  under  side 
for  some  time.  The  upper  side  may  be  polished  by  abrasion.  The 
exposed  end  of  a  root  undergoing  extrusion  is  also  sometimes  made 
smooth  by  abrasion.  A  bit  of  root  left  in  situ  after  breakage  during 
extraction  usually  undergoes  the  same  process  of  extrusion,  but  may 
not  decay  until  it  comes  under  oral  influences.  Usually  a  fistula  leads 
to  such  a  root,  but  verv  rarelv  the  jjum  mav  heal  over  it. 

Such  a  root  may  at  any  time  become  the  source  of  apical  abscess 
or  of  an  intractable  neuralgia. 


23 


CHAPTER    XIII. 

DENTAL  CARIES:  DIAGNOSIS,  SYMPTOMS,  AND  PROGNOSIS. 

HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS. 

Diagnosis  of  Dental  Caries. 

The  diagnosis  of  dental  caries  is  made  through  both  objective  and 
subjective  symptoms.  The  signs  are  the  existence  of  cavities  and 
of  softened  areas,  directly  visible  or  made  evident  through  instru- 
mental means.  The  symptoms  are  pains  of  several  degrees  of  inten- 
sity. The  nature  and  intensity  of  the  pains  furnish  a  guide  to  the 
depth  of  the  carious  invasion,  and  but  an  indirect  indication  of  the 
location  of  the  disease. 

Diagnosis  by  Objective  Symptoms. — The  presence  of  the  markings 
of  superficial  decay,  decalcified  surfaces,  or  cavities  may  often  be  de- 
tected at  a  glance  or  be  seen  reflected  in  a  mouth  mirror.  Opacity  of 
enamel  is  usually  due  to  its  superficial  decalcification  or  caries  beneath 
it,  though  at  times  a  malformation  may  exist.  The  discoloration  or 
opacity  about  a  fissure  should  excite  suspicion  of  caries.  In  the 
routine  examination  for  cavities,  sharp,  finely  pointed  explorers  bent 
at  various  angles  are  to  be  passed  over  all  the  surfaces  of  the  teeth. 
If  the  enamel  at  any  point  admit  the  point  of  the  explorer,  caries  is 
usually  present.  Fissures  are  sometimes  deceptive  in  this  respect. 
A  good  rule  is  to  adjudge  the  presence  of  caries  when  the  point  catches 
slightly  as  removed. 

In  the  search  for  approximal  caries  great  care  is  required,  explorers 
with  very  short  points  being  often  necessary,  as  long  points  will  not 
turn  into  the  cavity  owing  to  the  close  contact.  Frequently  a  cavity 
may  only  be  discoveral)le  from  one  point  of  access.  In  the  absence  of 
evident  cavities,  some  force  should  be  applied  to  detect  softened  spots 
of  enamel.  The  catching  of  the  explorer  upon  })oth  teeth,  after  it  has 
passed  through  the  interspace,  often  simulates  the  catch  in  a  cavity. 

Unwaxed  floss  silk  passed  over  carious  surfaces  indicates  a  rough 
surface  by  fraying.  It  may,  however,  at  times  pass  readily  over  a 
cavity  easily  detected  by  instruments;  so  that  it  is  not  absolutely 
reliable  as  a  test. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS        355 


Fig.  325 


The  strong  light  of  an  electric  mouth  lamp  transmitted  through 
the  teeth  exhibits  a  cavity  as  an  opaque  spot  outlined  upon  a  pinkish 
background.  It  not  only  permits  an  easy  diagnosis, 
but  also  affords  evidence  of  the  depth  of  penetra- 
tion. Mechanical  separators  or  wedges  are  at  times 
necessary  to  press  apart  contiguous  teeth  sufficiently 
to  admit  exploring  instruments. 

The  necks  of  the  teeth  should  be  examined  with 
sharp  points  to  note  any  softness  of  the  tooth  tissues. 
The  margins,  particularly  the  cervical  and  neigh- 
boring margins,  of  every  filling  should  be  ex- 
plored to  test  the  integrity  of  the  junction  of  fill- 
ing and  tooth  or  any  excess  or  deficiency  of  filling 
material. 

The  examination  should  be  conducted  by  one  of 
two  systematic  methods.  In  one  method  the  occlusal 
faces  of  all  the  teeth  are  first  examined  in  one  survey, 
then  the  interproximal  spaces,  and  lastly,  the  buccal 
and  lingual  surfaces  of  the  teeth.  In  the  other 
method  every  portion  of  each  tooth  is  examined, 
beginning  with  a  central  incisor  or  terminal  molar, 
before  passing  to  the  adjoining  tooth.  Any  cavity 
or  condition  found  should  be  noted  upon  a  diagram 
for  reference  at  sittings. 

Diagnosis  by  Subjective  Symptoms.— Com- 
plaints by  patients  that  cold  or  hot,  salt,  sweet,  or 
acid  substances  taken  into  the  mouth  cause  unlocal- 
ized  or  partly  localized  pain  indicate  exposed  and 
hypersensitive  dentine  or  pulp  exposure.  Such  com- 
plaint is  to  have  due  consideration. 

Pain  beginning  without  the  api)licati()n  of  spinal 
stimuli  is  likewise  ordinarily  connected  with  caries 
or  its  sequelse,  and  should  be  taken  into  account. 

Pain  produced  upon  mastication  has  either  the 
same  significance  or  is  a  symptom  of  pericemental 

Explorer  for  caries. 

irritation.  (Jack.>) 


Prognosis  of  Caries. 

If  existing  caries  be  promptly  treated  in  youth  and  a  proper  sys- 
tematic prophylaxis  be  employed,  its  recurrence  during  youth  may  be 


American  Text-book  of  Operative  Dentistry. 


356 


DENTAL  CARIES 

Fig.  326 


M 


Dow  electric  lamp  for  mouth  illumination,  with  reflectors.  Reflector 
A  is  jointed  to  vary  the  angle  of  reflection.  Reflector  B  is  for  illumi- 
nation of  the  fauces.     Reflector  C  is  for  lateral  illumination.     (Jack.i) 

largely  prevented.  At  about  adult  age  a  fair  degree 
of  immunity  may  be  expected.  In  the  absence  of 
treatment  or  prophylaxis  the  exciting  causes  seem  to 
become  very  active,  and  many  teeth  may  be  lost  from 
caries  or  by  reason  of  extraction  for  pulp  and  peri- 
cemental diseases.  Extraction  itself  brings  many 
evils  in  its  train. 

Even  advanced  caries  may  be  checked  by  proper 
filling  or  crowning,  and  if  then  prophylaxis  receive 
due  attention  the  prognosis  for  the  teeth  is  generally 
good;  indeed,  it  seems  as  though  but  few  conditions 
exist  dependent  upon  caries  alone  which  are  not  sub- 
ject to  correction  by  some  of  the  means  within  the 
resources  of  the  profession. 

Hypersensitivity  of  Dentine. 

The  exposure  of  dentine  to  external  agencies  is  so 
commonly  followed  by  an  increase  in  sensitivity  that 
the  condition  requires  description  in  itself.  It  is  a 
general  condition  attendant  upon  abrasion,  erosion, 
and  caries,  and  has  a  therapeutics  of  its  own. 

The  term  sensitive  dentine  applied  to  this  condition 
is  a  misnomer;  all  vital  dentine  is  sensitive,  and  its 
degree  of  sensitivity  differs  markedly  in  individuals; 
it  is  only  when  hypersensitivity  is  observed  that  the 
condition  becomes  pathological. 

Hypersensitivity  of  dentine  may  be  defined  as  such 


*  American  Text-book  of  Operative  Dentistry. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS      357 

a  degree  of  sensitiveness  of  the  dentinal  fibrils  as  interferes  with  the 
comfortable  excavation  and  shaping  of  a  cavity  of  decay;  or  whicii,  in 
the  absence  of  dental  ministrations,  causes  painful  symptoms,  as  a 
rule  reflected  about  neighboring  parts. 

Causes  and  Pathology. — Normally  the  dentine  is  protected  from 
external  agencies  by  the  enamel  and  in  the  early  stages  of  gum  recession 
by  the  cementum. 

With  the  removal  of  these  by  caries,  erosion,  abrasion,  or  fracture, 
the  terminal  filaments  of  the  dentinal  fibrils  become  subjected  to 
sudden  variations  of  temperature  ranging  from  a  little  above  32°  F., 
the  temperature  of  ice-water,  to  130°  F.,  that  of  very  hot  foods  or 
liquids. 

These  thermal  stimuli  at  times  give  evidence  of  their  effect  by 
producing  painful  sensations.  The  pulp  is  stimulated  through  the 
odontoblasts  and  their  relations  with  the  terminals  of  sensory  nerves 
in  the  pulp,  and  a  degree  of  vascular  overfulness  occurs  which  may 
be  denominated  mild  hyperemia.  The  effect  of  these  reactions  is  to 
cause  the  sensory  functions  of  the  pulp  to  become  somewhat  exalted, 
and  it  therefore  becomes  more  responsive  to  the  stimuli. 

Apart  from  the  effect  of  thermal  changes,  other  substances  act  as 
irritants.  The  lactic  acid  and  other  bacterial  products  in  the  cavity 
of  decay  without  doubt  play  a  part  in  exalting  the  irritability  of  the 
fibrils.  A  slightly  loosened  filling  holds  the  acid  in  contact,  as  such 
cases  are  often  very  sensitive.  Salt,  sweet,  or  acid  substances  intro- 
duced into  the  mouth  are  also  evidently  irritant,  as  active  symptoms 
follow  their  application  to  hypersensitive  dentine. 

Mechanical  abrasion  or  erosion  may  irritate  the  fibrils,  or  at  least 
expose  them  to  the  action  of  other  irritants.  As  a  rule,  however,  the 
abraded  or  eroded  surfaces  are  protected  from  hypersensitivity  by  the 
process  of  eburnation.     (See  Transparent  Zone.) 

The  scraping  of  necks  of  teeth  with  scalers  sometimes  induces 
exposure  of  dentine.  AVithin  cavities  of  decay  the  hypersensitivity  is 
greatest,  as  a  rule,  at  the  dentinal  periphery.  That  at  this  point 
the  dichotomous  endings  of  the  tubules  present  a  greater  number  of 
fibrils  to  the  action  of  the  irritant  is  quite  evident. 

In  cervical  hypersensitivity  the  cementum  or  enamel  is  removed  by 
abrasion,  erosion,  or  caries,  and  the  fibrils  are  exposed.  The  presence 
of  the  gramdar  layer  of  Tomes  in  this  situation,  and  the  possibility 
of  this  layer  containing  the  expansions  of  the  lil)rils,  are  to  l)e  con- 
sidered. 


358  DENTAL  CARIES 

In  certain  cases  the  irritation  excited  by  the  touch  of  an  instrument 
to  dentine  adjacent  to  enamel  is  carried  to  the  pulp  by  anastomosing 
dentinal  fibrils.  This  was  proved  by  a  few  cases,  of  which  the  follow- 
ing is  an  extreme  one : 

In  a  central  incisor  secondary  dentine  had  filled  a  portion  of  the 
pulp  cavity  (Fig.  327,  SD).  Caries  had  subsequently  removed  the 
incisal  portion  of  this  secondary  growth  and  also  the  dentine  contain- 
ing fibrils  leading  from  the  pulp  cavity  to  the  middle  of  the  incisal  edge. 
The  application  of  an  excavator  to  dentine  in  the  incisal  portion  of 
the  cavity  (at  A),  the  fibrils  of  which  could 
have  no  direct  relation  with  the  pulp,  pro- 
duced flashes  of  pain.  This  was  unmistak- 
ably of  the  character  of  hypersensitive  dentine. 
A  professional  friend  claimed  to  feel  sensi- 
tivity in  a  cervicolingual  cavity  of  a  molar  in 
which  the  filaments  had  been  destroyed  by 
suppuration  for  one-third  of  the  length  of  the 
canals.  If  his  contention  was  true,  the  sensa- 
,  ,.    ^  ,         .  .       f     tion  must  have  been  conducted  by  way  of  the 

Indirect    transmission    ot  J  J 

sensation  in  a  case  of  hyper-     granular  layer  of   Tomcs  to  the  level  of  the 

sensitive  dentine:  SD,  sec-  ,  ,       ,  ,  i  r^i     -i       ,        •,  i 

ondary  dentine:  A,  point  of     pulp   and    thcucc    by   the    hbrils  to  its  sub- 

hypersensitivity.  (Diagram-       stance 
matic.) 

Spots  of  cervical  hypersensitivity  have  been 
occasionally  recorded  as  occurring  in  teeth  the  canals  of  which  have 
been  filled. 

Head*  records  a  case  in  which  the  dentine  bounding  the  pulp  canal 
remained  hypersensitive  for  a  year  after  the  pulp  was  removed.  In 
this  connection  the  possibility  of  the  presence  of  a  vital  pulp  filament 
in  the  pulp  canal,  or  of  irritable  apical  tissue  receiving  the  impact  of 
liquid  forced  down  upon  it  by  a  canal  probe,  or  of  a  pericementum 
irritable  to  touch  of  any  sort,  must  all  have  due  differentiation.  I 
have  never  seen  a  case  of  hypersensitivity  of  dentine  in  which  some 
filament  of  pulp  was  not  present  in  at  least  a  part  of  the  tooth. 

Dentine  cannot  become  inflamed  in  the  ordinary  sense,  as  leukocytes 
cannot  enter  the  tubules;  nevertheless,  the  irritability  of  the  fibrils, 
like  that  of  other  protoplasm,  may  be  exalted  (or  lessened).  It  has 
been  noted  that  during  excavation  of  a  cavity  the  irritability  is,  as  a 
rule,  greatest  at  the  surface  of  the  dentine — I.  e.,  at  the  point  at  which 
irritants  are  present  in  greatest  amount  and  the  fibrils  most  numerous. 

•  Dental  Cosmos,  1899. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     359 

With  hypersensitivity  other  functions  ar(*  increased,  and  in  con- 
ditions produciniif  a  constant  stimulation  a  constructive  change  may 
occur  and  the  fil)ril.s  form  tulndar  substance  at  their  own  expense. 
(See  Transparent  Zone  and  Tubular  Calcification.) 

That  the  hypersensitivity  is  primarily,  as  a  rule,  a  disease  of  the 
fibrils  involved  or  of  the  fibrils  and  their  odontoblasts  is  shown  by  the 
fact  that  occasionally  of  two  cavities  in  the  same  tooth  one  will  present 
a  hypersensitivity  and  another  none;  again,  one  part  of  a  cavity  may 
be  hypersensitive  and  the  rest  not  so.  In  other  cases  perfectly  normal 
dentine  is  hypersensitive,  as  noted  when  the  attempt  is  made  to 
reduce  a  sound  tooth  for  bridge-work  or  a  sound  fissure  is  opened  for 
prevention  of  decay. 

There  are  two  theories  accounting  for  the  transmission  of  the 
impulse  which  is  translated  by  the  patient  as  pain:  (1)  That  a  con- 
traction of  the  whole  cell,  fibril  and  odontoblast,  occurs,  the  sensory 
nerve  endings  being  pressed  upon  in  the  act.  (2)  That  a  wave- 
like motion  along  the  protoplasm  is  set  up,  causing  excitation 
of  the  sensory  nerves  and  due  to  the  incompressibility  of  the  water 
(Gysi). 

The  first  is  analogous  to  the  contraction  of  a  voluntary  muscle 
cell  under  nerve  impulse.  The  whole  muscle  cell  contracts,  though 
the  nerve  ending  is  supplied  to  only  a  portion  of  it.^ 

This  hypothesis  fits  the  symptoms  as  excited  by  both  mechanical 
and  chemical  irritants,  while  the  second  theory  does  not. 

Symptoms. — A  certain  degree  of  uneasiness  of  undefined  character 
may  at  times  be  noted  in  teeth  containing  cavities,  but,  as  a  rule,  pain 
other  than  pulp  pain  is  only  felt  upon  the  application  of  stimuli.  In 
some  cases  the  exposure  of  dentine  about  the  necks  of  teeth  may 
induce  such  an  unbearable  local  pain  or  neuralgic  condition  as  to 
positively  demand  relief. 

The  infiltration  of  acid,  salt,  or  sweet  substances  into  contact  with 
a  hypersensitive  surface  is  followed  by  a  wave  of  gnawing  pain  reflected 
usually  along  the  course  of  contiguous  nerve  filaments.  While  not 
definitely  localized,  owing  to  the  fact  that  the  pulp  does  not  possess 
a  tactile  or  localizing  sense,  the  pain  may  usually  be  referred  to  a 
certain  part  of  the  mouth.  The  pressure  of  an  instrument  upon  the 
dentine  is  attended  by  a  flash  of  sharp  ])ain,  which  continues  for  a 
time,  but  lessens  if  the  contact  be  maintained.  In  this  test  the  pain 
is  localized  in  the  aft'ected  tooth,  the  touch  of  the  instrument  being 

'  Black,  American  System  of  Dentistry. 


SCO  DENTAL  CARIES 

followed  by  a  recognition  of  position  by  the  tactile  organ  of  the  tooth, 
the  pericementum. 

Occasionally  food  forced  by  mastication  against  a  hypersensitive 
surface,  such  as  due  to  abrasion  or  caries  in  a  crevice,  will  produce 
a  sharp  pain  subsiding  promptly,  and  which  may  not  be  repeated  for 
some  time. 

Cavities  dried  for  filling  usually  produce  a  steady  pain,  caused  by 
dryness  and  relieved  by  an  analgesic  or  by  filling. 

It  is  beyond  doubt  that  individuals  difi'er  u  ^.  to  the  degrees  of  normal 
dentinal  sensitivity;  the  dentine  of  one  person  may  be  cut  freely  without 
evidence  of  maTked  pain;  in  another  the  touch  of  an  instrument  to  the 
newly  exposed  dentine  is  productive  of  unbearable  pain.  The 
difference  in  degree  of  irritability  is  manifested  in  another  manner: 
if  a  mild  sedative — for  example,  oil  of  cloves — be  applied  to  the  hyper- 
sensitive dentine  of  one  person,  it  may  remove  the  distressing  symp- 
toms, but  with  others  it  may  be  necessary  to  employ  the  most  extreme 
measures  to  reduce  in  any  degree  the  hypersensitivity. 

In  a  few  cases  enamel  has  exhibited  sensitivity.  In  one  case  the 
effort  to  open  sound  fissures  about  a  cavity  for  prevention  excited  sharp 
pain,  ceasing  upon  removal  of  the  instrument.  The  patient  was, 
however,  a  sufferer  from  insomnia  and  from  the  effects  of  morphine 
taken  for  it,  and  her  dentine  was  exquisitely  sensitive. 

In  another  patient  the  side  of  the  enamel  exposed  by  a  cavity  in  a 
molar  analogous  to  that  in  Fig.  327  gave  flashes  of  pain  when  touched 
with  an  excavator  point,  though  no  evident  direct  path  of  transmission 
to  the  pulp  could  be  seen.  Caush's  tubes  and  indirect  transmission 
seem  the  only  basis  of  explanation. 

There  is  a  pseudohypersensitivity  of  enamel  in  some  cases  due  to 
apprehension.  The  patients  can  be  ridiculed  out  of  the  idea  by  demon- 
strating its  absurdity,  as,  for  example,  by  touching  a  cusp  and  then 
showing  them  the  part  touched.  Pericemental  irritability  at  times 
must  also  be  excluded. 

There  can  be  no  question  that  systemic,  nervous  irritability  from  any 
cause  aggravates  the  phenomenon  of  hypersensitivity,  though  whether 
it  can  make  dentine  more  sensitive,  or  whether  the  patient  is  less 
able  to  endure  pain,  is  not  clear. 

The  general  perceptivity  of  the  individual  seems  to  play  a  part,  and 
even  apparently  normal  dentine  may  be  exquisitely  hypersensitive. 
Again,  pain  j)roduced  in  excavating  may  be  due  to  the  character  of 
the  manipulation,  heavy  continued  biin-ing  producing  heat;  lighter 


HYPERSENSITIVE  DEXTIXK  AND  ITS  THERAPEUTICS     361 

touches  may  excavate  equally  well,  but  produce  much  less  pain.     The 
(lulness  of  the  excavator  or  bur  has  a  similar  effect. 

Diagnosis. — In  the  diagnosis  the  above  characteristic  symptoms  are 
to  be  considered.  The  decisive  test  is  made  by  pressing  an  instrument 
upon  the  suspected  surface,  when  the  characteristic  pain  is  produced, 
subsiding  upon  or  shortly  after  removal  of  the  contact. 

Upon  the  pulpal  wall  of  deep  cavities  doubt  may  exist  as  to  whether 
the  pain  is  due  to  pulp  irritation. 

A  suspected  exposure  may  be  differentiated  by  the  localization  of 
the  pain  upon  touch  to  a  point  corresponding  to  the  pulp  horn  or 
pulp  body,  or  by  the  point  catching  in  the  exposure.  Hyper- 
sensitive dentine  will  be  more  generally  distributed  or  occur  at 
points  at  which  exposure  is  impossible.  Pulp  abnormality  or 
approach  may  be  detected  by  means  of  a  drop  of  cool  water  or  a 
blast  of  cool  air  from  a  syringe.     (See  Hyperemia  of  the  Pulp.) 

Treatment. — The  methods  of  treatment  which  have  been  followed 
for  the  relief  of  hypersensitivity  of  dentine,  and  the  induction  of  such  a 
degree  of  analgesia  as  will  permit  the  necessary  cutting  of  dentine, 
may  be  divided  into  general  and  local. 

General  Remedies. — The  general  remedies  employed  are  those 
which  abolish  or  lessen  the  perceptive  function  in  the  centres  of  the 
fifth  pair  of  nerves,  or  which  reduce  hyperirritability  of  the  nervous 
system.  Either  general  anesthesia  or  general  anodynes  are  employed 
to  lessen  perception.  The  inhalation  of  a  few  whiffs  of  chloroform 
or  ethylic  ether  lessens  the  perception  of  pain.  Chloroform  is  usually 
avoided  in  this  connection  on  account  of  its  dangers  when  used  in  the 
sitting  position.  Slight  etherization,  the  inhalation  being  carried  only 
to  the  benumbing  point,  affords  marked  relief  from  the  pain  inci- 
dental to  the  cutting  of  hypersensitive  dentine.  Nitrous  oxide  and 
oxygen  have  been  employed  with  some  satisfaction,  administered  by 
means  of  a  nasal  apparatus,  which  permits  the  mouth  to  be  unob- 
structed. 

The  administration  of  general  anodynes,  particularly  the  combina- 
tion of  morphine  and  atropine,  has  been  found  us(>ful  in  tiiis  field: 

I^. — Morphina"  sulph •?•"•  8 

Atropine  sulph gr.  j\^ 

M.  et  ft.  pil.  No.  1. 

Sig. — To  be  taken  <iiie-half  liour  beforo  operation. 

Flagg  noted  that  blondes  bear  morphine  sulphate  better  than 
brunettes;  particularly  are  nervobilious  and  bilionervous  patients 
idiosyncratically  opposed   to  its  use,  the  physiological  action  of  the 


362  DENTAL  CARIES 

drug  being  reversed  or  the  after-effects  being  pronounced.  Patients 
having  dark  hair  and  bhie  eyes  may  be  expected  to  be  thus  idio- 
syncratic. For  them  he  recommended  morphine  bimeconate  sohi- 
tion  in  doses  equivalent  to  j  grain  of  the  salt,  to  be  taken  one  the 
evening  before  and  the  other  before  the  operation. 

Chloral  in  5-  or  10-grain  doses,  administered  in  water  before  the 
operation,  has  a  quieting  effect  upon  the  nervous  system.  Ambler^ 
has  suggested  the  use  of  from  10  to  20  drops  of  fluid  extract  of 
piscidia  erythrina,  to  be  administered  about  ten  minutes  before  oper- 
ating. Drowsiness  may  be  expected.  Phenobromate,  10  grains, 
before  operation,  or  15  grains  for  any  great  pain,  may  be  admin- 
istered in  a  copious  draught  of  water. 

Hyoscyamine  hydrobromate,  -^^  grain,  will  be  useful  in  those  cases 
which  are  associated  with  muscular  spasm  or  hysteria. 

The  coal-tar  derivatives,  phenacetin,  acetanilide,  and  others,  are 
occasionally  efficient.  The  preparations  known  as  antikamnia  (said 
to  be  a  combination  of  acetanilide,  caffeine  citrate,  and  sodium 
bicarbonate)  and  ammonol  (acetanilide  and  ammonium  carbonate, 
equal  parts)  are  to  be  preferred  in  this  connection.  The  dose  of 
the  latter  two  is  10  grains,  administered  one-half  hour  before 
operation. 

The  induction  of  the  hypnotic  state  belongs  in  the  category  of  means 
acting  upon  the  nerve  centres.  The  use  of  the  ordinary  suggestion 
that  the  work  will  not  be  unduly  painful,  considerate  treatment, 
patience,  and  the  employment  of  remedies  all  have  a  calming  influ- 
ence, permitting  relaxation  upon  the  part  of  the  patient,  who,  if  "  keyed 
up"  to  expect  great  pain,  will  expect  and  feel  unduly. 

The  use  of  blue-light  anesthesia  consists  in  causing  the  patient  to 
gaze  intently  for  a  few  minutes  at  a  blue-globed  electric  light  having 
a  reflector  behind  it.  A  blue  veil  is  thrown  about  the  head  and  lamp  to 
exclude  daylight.  Short  operations  have  been  performed  under  its  seda- 
tive, or,  possibly,  hypnotic  effects,  though  it  seems  to  fail  in  some  cases. 

Local  Treatment. — The  local  treatment  of  hypersensitive  dentine 
may  be  considered  from  two  standpoints,  according  to  whether  a 
concavity  containing  it  requires  excavation,  or  whether  the  hyper- 
sensitive spots  are  not  to  be  excavated  after  treatment. 

Treatment  in  Cavities  of  Decay. — The  remedies  employed  in 
the  endeavor  to  reduce  or  abolish  hypersensitivity  in  a  cavity  of  decay 

'  Dental  Cosmos,  1901.  » 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     363 

at  the  time  of  operation  are  quite  numerous;  few  are,  however,  always 
effective.     They  may  be  classed  under  two  headin^js: 

1.  Those  which  temporarily  benumb  or  anesthetize  the  Hbrillie  and 
prevent  the  transmission  of  sensation. 

2.  Those  which  chemically  destroy  the  fibrillae  for  a  distance,  thus 
preventing  transmission  of  sensation. 

Remedies  whicu  Benumb  the  Fibrill.e. — Chief  among  these  for 
its  universality  of  application  is  dryness.  Dentine,  which  protests 
against  even  the  touch  of  an  instrument  while  wet,  has  its  sensitivity 
so  lessened  after  the  application  of  a  rubber  dam  and  drying,  that  it 
may  be  cut  freely,  in  many  cases  without  the  aid  of  medicinal  agents. 
So  well  is  this  recognized  that  isolation  and  drying  of  teeth  are  regarded 
as  a  necessary  preliminary  to  cavity  preparation.  The  degree  of 
insensitivity  induced  is  in  proportion  to  the  dryness.  The  drying 
temporarily  deprives  the  dentinal  protoplasm  of  a  portion  of  its  water 
and  inhibits  the  transmission  of  sensation  by  reducing  functional 
activity. 

A  continuous  blast  of  air  passed  from  a  compressed-air  apparatus 
through  a  heated  metal  bidb  and  nozzle,  or  through  an  electrically 
heated  coil,  should  be  employed  until  the  dentine  is  desiccated.  This 
is  evidenced  by  its  extreme  whiteness.  Other  forms  of  hot-air  syringes 
may  be  substituted  with  less  satisfaction  and  greater  fatigue  to  the 
operator. 

The  application  of  absolute  alcohol  assists  the  drying  because  of 
its  affinity  for  water.  The  addition  of  a  little  menthol  to  the  alcohol 
assists  by  anesthetic  action.  The  pain  from  the  warm  air  may  at  first 
be  quite  severe,  l)ut  even  in  greatly  hypersensitive  cases  the  norzle  of 
the  syringe  may  soon  be  approximated  to  the  cavity,  though  in  some 
cases  it  may  be  necessary  to  make  an  application  of  a  mixture  of 
equal  parts  of  carbolic  acid  and  oil  of  cloves,  or  of  gum  camphor  and 
carbolic  acid  (phenol  camphor),  both  of  which  have  some  anesthetic 
effect.  Menthol  maybe  added  to  either.  When  desirable  their  effect 
may  be  hastened  by  pressure  with  unvulcanized  rubber. 

An  instrument  known  as  the  "deliydrator"  causes  absolute  alcohol 
placed  in  a  special  chamber  between  the  bulb  of  the  hot-air  syringe 
and  the  nozzle  to  be  vaporized  upon  the  hypersensitive  dentine. 
The  drying  effect  is  thereby  augmented  and  the  dentine  satisfactorily 
obtunded. 

Some  degree  of  dryness  is,  as  a  rule,  a  necessary  preliminary  to 
success  with  other  applications. 


364  DENTAL  CARIES 

Following  dryness,  the  excavation  should  be  done  with  sharp 
instruments  and  burs.  The  latter  should  only  be  lightly  touched  to 
the  dentine  and  be  revolved  at  high  speed.  Letting  the  bur  occasion- 
ally run  free  cools  it.  The  heat  of  friction  is  considerable  and  highly 
irritating. 

Refrigeration  by  a  spray  of  ether  or  ethyl  or  methyl  chloride  reduces 
the  temperature  of  the  fibrils  and  pulp,  benumbing  them.  The 
rubber  dam  should  be  applied  to  isolate  the  teeth  operated  upon. 
Ether  is  applied  by  means  of  a  double-bulbed  atomizer;  the  chlorides 
are  contained  in  glass  tubes  conveniently  capped.  The  cap  being 
raised,  the  heat  of  the  hand  causes  vaporization  of  the  agent  within 
the  tube,  which  forces  the  liquid  out  of  the  orifice  of  the  tube  in  a  fine 
but  forcible  stream.  A  spraying  nozzle  is  also  obtainable.  The  cavity 
should  at  first  contain  a  pellet  of  cotton  in  order  that  the  dentine  may 
be  gradually  obtunded  and  painful  response  on  the  part  of  the  pulp 
avoided. 

"  Vapocain"  and  "potassocain,"  proprietary  agents  which  consist  of 
a  15  per  cent,  solution  of  cocaine  in  ether,  are  applied  to  hypersensitive 
dentine  upon  the  theory  that  the  ether  enters  the  tubules,  carrying 
the  cocaine  into  contact  with  the  fibrils;  the  ether  evaporates,  leav- 
ing the  cocaine  in  aqueous  solution  to  benumb  them.  This  requires 
several  minutes.  They  are  useful  in  the  deeper  cavities.  Jack 
recommends  that  the  cavity  acidity  be  neutralized  before  their 
application.^ 

A  10  to  25  per  cent,  solution  of  cocaine  in  water  may  be  forced  into 
the  tubules  by  applying  it  on  a  pellet  of  amadou,  placing  over  this  soft 
vulcanite  rubber  and  producing  pressure  with  a  burnisher  for  from 
three  to  six  minutes.  The  pressure  should  be  gradually  applied.  A 
gratifying  degree  of  dentinal  anesthesia  may  often  be  obtained. 

Adrenalin  chloride  solution  1  to  1000  plus  chloretone^  or  cocaine  has 
been  used  in  this  manner  with  some  effect. 

Miller^  has  shown  that  by  taking  a  modelling  composition  impres- 
sion of  the  cavity,  then  applying  a  few  threads  of  cotton  saturated 
with  cocaine  to  the  floor  of  the  cavity,  then  placing  a  thickness  of 
rubber  dam  over  the  entire  cavity  surface,  replacing  the  modelling 
composition  and  producing  pressure,  anesthesia  can  be  produced  when 
there  is  not  a  greasy  condition  of  the  cavity,  nor  thick  layers  of 
decalcified  dentine  nor  much  secondary  dentine  present. 

'   American  Text-Vjrjok  oi  Operative  Dentistry.  *  Parke,  Davis  &  Co. 

^  Dental  Review,  1900. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     365 

Cataphorcsis  (Greek  kata,  down,  and  phoreo,  I  l)ear  or  bring)  is, 
in  technical  parlance,  the  transference  of  substances  from  the  anodal 
or  positive  pole  of  a  battery  toward  the  cathodal  or  negative  pole. 
They  are  thus  carried  into  the  tissues. 

Cataphoresis  is  to  be  distinguished  from  electrolysis,  by  which 
substances  are  decomposed  and  their  elements  carried  from  positive 
to  negative  or  from  negative  to  positive  poles,  according  to  their 
polarity.  In  cataphoresis  a  substance  is  carried  unchanged  from  the 
positive  toward  the  negative  pole,  after  the  manner  of  granules  in 
protoplasm  acted  upon  by  the  same  force.     (See  Chapter  I.) 

As  applied  to  dentistry,  a  primary  current  from  a  battery  arranged 
with  the  cells  in  series  has  the  positive  pole  or  conductor  connected 
with  a  resistance  or  current  controller  capable  of  being  so  manipulated 
as  to  gradually  reduce  the  resistance  to  the  current  a  fraction  of  a  volt 
at  a  time.  This  is  called  a  "fractional  volt  selector."  This  is  usually 
a  broken  ring  of  graphite,  to  one  end  of  which  the  incoming  current  is 
admitted  by  means  of  the  conducting  cord  and  travelling  indicator; 
at  the  other  end  the  current  passes  out  by  a  similar  cord,  which  in  turn 
is  attached  to  a  milliamperemeter  or  instrument  recording  the  quantity 
of  current  passing  through  the  circuit.  From  this  a  cord  leads  to  the 
positive  electrode  applied  to  the  tooth  cavity.  To  the  face,  neck,  or 
wrist  of  the  patient  a  moist  electrode  (negative)  is  applied,  which  by 
its  conducting  cord  leads  the  current  back  to  the  negative  pole  of  the 
battery. 

It  will  be  seen  that  the  current  passes  in  turn  from  the  positive 
pole  of  the  battery  to  the  resistance,  to  the  recording  instrument,  to 
the  patient  (another  resistance),  to  the  battery,  completing  the  circuit. 
These X are  said  to  be  arranged  in  series. 

In  the  use  of  the  cataphoric  apparatus  the  tooth  is  securely  insulated 
by  well-ligatured  rubber  dam  and  cotton  saturated  with  a  solution 
of  cocaine  hydrochlorate  or  citrate  of  a  strength  of  from  10  per  cent, 
to  a  saturated  solution  is  placetl  in  the  cavity.  The  platinum  anode 
is  wrapped  with  cotton,  dipped  in  the  solution,  and  inserted  into 
contact  with  the  cotton  in  the  cavity.  The  controller  is  now  so  ma- 
nipulated as  to  gradually  cut  out  its  resistance  to  the  current,  and  the 
high  resistance  of  the  dentine  is  gradually  overcome. 

The  cocaine  solution  should  be  renewed  as  dryness  occurs,  as  dryness 
increases  the  resistance.  The  cocaine  is  carried  along  the  fibrils  to 
the  pulp  by  the  electric  current,  and  dentinal  followed  by  pulpal 
anesthesia  results. 


366  DEXTAL  CARIES 

From  eight  to  fifteen  minutes,  or  sometimes  longer,  are  required 
for  dentinal  anesthesia,  which  loss  of  time  is  largely  regained  in  the 
facility  of  operation.^ 

Price^  has  shown  that  pulp  anesthesia  is  gained  more  readily  by 
concentrating  the  action  of  the  cocaine  upon  the  pulpal  wall  by  means 
of  a  small  electrode.  If  general  dentinal  anesthesia  is  required  he 
prefers  this  method,  as  the  pain  receptivity  of  the  pulp  is  abolished. 
A  broader  application  anesthetizes  the  dentine. 

Woodward^  has  shown  that  in  the  latter  case  the  dentine  in  a  cavity 
upon  the  opposite  side  of  a  tooth  being  operated  upon  may  remain 
sensitive. 

The  pulp  may  be  anesthetized  by  this  method  for  removal.  In 
difficult  conditions  this  is  a  very  valuable  means  of  therapeutics. 

The  pulp  is  not  injuriously  affected  in  ordinary  applications,  unless 
saturated  by  long  application.  A  reaction  resulting  in  hyperemia  may 
take  place.  To  obviate  this,  the  pulp  should  not  be  oversaturated,  the 
fibrils  should  be  treated  with  carbolic  acid,  and  in  deep  cavities  a 
non-conductor  should  be  used  before  filling. 

In  case  absolute  insensitivity  is  produced  the  anatomy  of  the  pulp 
must  carefully  be  considered,  so  that  it  be  not  exposed  during  the 
excavation  of  the  cavity.  Insulation  of  the  pulp  from  thermal  shock 
subsequent  to  filling  is  also  to  have  consideration. 

The  pulp  may  have  cocaine  forced  into  it  by  means  of  a  powerful 
compound-pressure  syringe.  The  Meyers  syringe  is  one  of  the  best. 
It  is  filled  with  a  5  to  15  per  cent,  solution  of  cocaine  in  water;  a 
convenient  drill  pit  is  made  with  a  No.  ^  bur;  the  nozzle  of  the  filled 
syringe  freed  of  air  is  forced  into  the  opening  and  continuous  or 
intermittent  pressure  produced  without  releasing  the  point  for  several 
minutes.  No  general  cavity  anesthesia  will  result  until  the  cocaine 
solution  has  infiltrated  the  area  of  pulp  underlying  the  fibrillar  connec- 
tions with  the  pulp.  The  forcing  of  cocaine  into  so  delicate  a  tissue 
may  produce  expansive  pressure,  and  may  cause  a  later  pulp  reaction, 
as  cocaine  is,  to  a  degree,  a  protoplasmic  poison.  The  method  is 
useful  in  pidp  extirpation  rather  than  in  hypersensitivity,  but  has 
occasional  use,  especially  in  cervical  cavities.  Secondary  dentine  is 
difficult  of  penetration,  and  gradual  approaches  must  be  made. 

In  another  use  of  cocaine  a  1  per  cent,  solution  may  be  injected  with 
a  hypodermic  syringe  into  the  gum  over  the  apex  of  the  root  of  a  tooth, 

'  Jack,  Amerioan  Text-V)ook  of  Operative  Dentistry. 

2  Dental  Summary,  April,  1903. 

'  International  Dental  Journal,  November,  1902 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     367 

the  object  being  to  paralyze  the  sensory  nerve  leading  from  the  pulp. 
It  is  not  without  danger  to  the  heart,  tliougli  it  may  be  resorted  to 
under  proper  precautions,  such  as  using  adrenalin  with  the  cocaine, 
administering  food  before  the  operation,  as  an  empty  stomach  is  an 
element  of  danger,  the  administration  of  aromatic  spirits  of  ammonia, 
coffee,  or  l)randy  before  operating.     Other  anesthetics  are  also  used. 

The  addition  of  adrenalin  to  the  cocaine  inhibits  the  absorption  of 
cocaine  from  the  point  of  injection;  also  acts  as  a  cardiac  stimulant. 
Five  drops  of  a  1  per  cent,  solution  of  cocaine  should  be  a  maximum 
dose,  and  should  be  injected  for  posterior  teeth  into  the  alveolar 
gum  to  anesthetize  the  nerve  trunk;  in  anterior  teeth  a  subgingival 
injection  is  sufficient.     (Honigmann  after  Braun.^) 

The  introduction  of  a  5  or  10  per  cent,  solution  of  cocaine  upon  cot- 
ton into  the  nostril,  upon  the  side  of  operation,  is  endorsed  by  Peck,  of 
Chicago,  as  a  means  of  anesthetizing  the  nerve  trunk  leading  from 
the  upper  incisors. 

Soderberg'  has  shown  that  painless  excavation  of  cavities  otherwise 
uncontrollable  may  be  effected  by  the  use  of  nervocidine,  an  alkaloid 
obtained  by  Dr.  D.  Dalma  from  the  East  Indian  plant  gasu-ba^u. 
Twenty-four  hours  are  required  for  complete  dentinal  anesthesia 
without  pulp  anesthesia  uidess  a  second  application  be  matle. 

The  primary  effect  of  nervocidine  being  irritating,  Soderberg  rec- 
ommends the  additional  use  of  cocaine,  both  being  mixed  with  zinc 
sulphate  cement. 

I^. — Gum  arable 5J 

Zinc  sulphate gss 

Water fSJ— M. 

Dissolve  the  zinc  sulphate  in  the  water,  add  the  gum  arabic,  stir;  let  stand  for  twenty-four 
hours  and  strain. 

I^. — Of  above  solution f  5ij 

Nervocidine gr.  x 

Cocaine  liydrochlorate gr.  x — M. 

To  a  portion  of  the  latter  .solution  add  uncalcined  zinc  oxide  to 
make  a  cement,  which  is  placed  in  the  dried  cavity.  Uncalcined  zinc 
oxide  added  to  the  first  formula  makes  zinc  sulphate  cement.  After 
excavation  the  acidity  of  the  nervocidine  should  be  neutralized. 
Buckley^  has  reconmiended : 

I^. — Menthol gr.  xx 

Chloroformi fjss 

Etheris f5j — M. 

Sig. — Place  a  little  in  the  cavity  after  the  rubber  dam  is  adjusted. 

'  Dental  Cosmos,  1905,  p.  1385.  -  Ibid.,  .\ugust,  1903. 

3  Ibid.,  1907.  p.  328. 


368  DENTAL  CARIES 

Hot  water  supplied  by  a  tube  leading  from  a  coil  heated  by 
electricity  and  attached  to  the  water  supply  pipe  of  the  fountain 
cuspidor  has  been  recommended  by  A.  F.  Merriman,  Jr.,  for  the 
obtunding  of  hypersensitive  dentine  in  cases  in  which  dryness  is  not 
readily  obtainable,  nor  immediately  nor  subsequently  desirable. 

It  is  claimed  that  satisfactory  analgesia  is  obtained,  and  that  the 
mucous  membrane  of  the  mouth  is  not  unduly  uncomfortable,  even 
when  the  heat  is  objectionable  to  the  finger  of  the  operator.  The 
advantages  of  the  method  for  excavation  and  grinding  are  obvious 
and  most  useful,  particularly  for  trimming  live  teeth. 

Remedies  which  Chemically  Destroy  the  Fibrils  for  a  Dis- 
tance, Preventing  Transmission  of  Sensation. — Agents  which 
chemically  destroy  the  dentinal  protoplasm  form  the  most  extensive 
group  of  dentinal  obtundents.  They  include  salts  of  metals,  such 
as  zinc  chloride  and  silver  nitrate;  carbolic  acid  and  its  derivatives, 
and  like  bodies;  the  cresols,  etc.;  mineral  acids,  notably  sulphuric, 
chromic,  and  nitric;  organic  acids — trichloracetic  and  lactic  acids — 
(full  strength);  alkalies — sodium  and  potassium  hydrates  and  car- 
bonates. 

Zinc  chloride,  silver  nitrate,  and  carbolic  acid  all  cause  coagulation 
of  the  fibrils  of  the  dentine.  The  mineral  and  organic  acids  chemi- 
cally decompose  both  protoplasm  and  the  calcified  tissues.  The 
concentrated  alkalies  chemically  destroy  protoplasm  and  bring 
about  its  quick  dissolution.  Like  all  active  chemical  substances,  the 
extent  of  their  action  depends  upon  the  freedom  with  which  they 
are  applied. 

The  application  of  any  of  these  agents,  as  a  rule,  causes  pain,  the 
degree  of  suffering  being  usually  in  proportion  to  the  depth  of  the 
cavity.  For  this  reason  the  more  powerful  agents,  like  zinc  chloride 
and  nitric  acid,  are  to  be  confined  to  cavities  of  moderate  depth,  while 
carbolic  acid,  especially  in  combination  with  the  oil  of  cloves,  may  be 
used  in  the  deeper  ones. 

Fused  zinc  chloride  is  used  in  its  deliquesced  form,  and  is  most 
active  when  some  of  the  salt  is  still  undissolved  in  the  bottle.  Its 
pain  in  suitable  cavities  is  a  fidl,  bearable  one,  gradually  increasing, 
sometimes  in  waves,  initil  a  crisis  is  reached,  when  the  pain  gradually 
ceases.  It  has  a  double  action,  not  only  coagulating  protoplasm, 
but  combining  with  its  water  owing  to  its  affinity  for  the  latter. 
On  account  of  this  property  its  action  may  be  limited  by  warm 
water. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     369 

An  undue  action  of  the  zinc  chloride  is  indicated  by  a  throbbing 
pain;  this  indicates  that  the  pulp  has  been  irritated.  When,  as  occa- 
sionally occurs,  no  pain  is  produced,  no  obtundent  effect  is  obtained. 
If  this  occur  regularly  the  drug  is  oversaturated  with  water. 

Bogue  has  suggested  that  cocaine  crystals  be  incorporated  with  the 
chloride  of  zinc  as  a  means  of  alleviating  the  pain  incident  to  the 
application. 

Miller,  following  Hoffheinz,  advocated  the  use  of  equal  parts  of 
zinc  chloride  and  chloroform. 

Certain  moderately  deep  cavities  may  be  filled  with  oxychloride  of 
zinc  cement,  the  free  zinc  chloride  acting  as  an  obtundent.  This 
requires  a  prolonged  action  and  is  only  resorted  to  in  cases  which  do 
not  admit  of  immediate  work,  or  in  which  procrastination  is  desirable. 

A  formula  of  wide  renown  is  known  as  Robinson's  remedy;  this 
may  be  made  in  one  of  two  ways: 

I^. — Potassium  liydrate 
(or  Sodium  liydrate). 

Carbolic  acid a  a — M. 

Reduce  the  gelatinous  mass  formed  with  alcohol. 

Or, 

I^. — Sodium  hydrate  (deliquesced), 

Calvert's  crystal  carbolic  acid a  a — ^M.     (Huey.) 

The  liquid  formed  is  spoiled  when  it  effloresces  upon  the  sides  of  the  bottle  neck. 

The  painfully  caustic  action  of  the  sodium  or  pota.ssium  hydrate 
is  modified  by  the  carbolic  acid. 

The  application  of  Robinson's  remedy  is  useful  in  the  simpler 
cavities  and  about  the  undecayed  but  hypersensitive  necks  of  teeth. 

If  this  remedy  or  zinc  chloride  be  required  about  the  periphery  of 
deep  cavities  the  plan  suggested  by  Jack,  of  varnishing  the  cavity 
floor  with    chloropercha  as  an    iinjXMietrable  protective  is  valuable. 

A  method  similar  to  the  use  of  Robinson's  remedy  consists  in  apply- 
ing carbolic  acid  to  a  cavity  and  then  without  removing  it  placing  a 
few  granules  of  .sodium  dioxide.^  Sodium  dioxide  alone  in  a  slightly 
moist  cavity  liberates  nascent  sodium  hydrate  (also  ILO,),  which  will 
destroy  the  gum  protoplasm  and  is  somewhat  effective  in  hypersensi- 
tive dentine. 

The  combination  of  potas.siuin  carbonate  with  glycerin  makes  a 
water-extracting  combination  having  but  little  coagulating  power. 
For  this  reason  it  may  be  used  in  the  deeper  cavities,  but  not  in  cases 
of  almost  exposed  pulp,  as  in  such  cases  its  application  is  painful. 

'  II.  J.  Moore,  Dental  Heview,  1906. 

24 


370  DENTAL  CARIES 

I}. — Potassium  carbonate gr.  xv 

Glycerin f5J- 

Mix  in  a  mortar. 

To  be  applied  on  a  pellet  of  cotton.     (Flagg.) 

It  may  be  used  with  effect  even  upon  slightly  moist  dentine. 

Not  being  escharotic  to  the  gum,  this  remedy  is  exceedingly  useful 
about  the  sensitive  but  undecayed  necks  of  teeth,  and  may  be  freely 
applied  after  moderate  drying  of  the  parts. 

If  necessary,  the  patient  may  be  given  the  prescription  and  directed 
to  apply  by  means  of  a  clean  tooth-pick,  which  should  not  be  used 
a  second  time,  as  the  mixture  may  be  infected  and  spoiled. 

Its  pain  simulates  that  of  zinc  chloride,  but  is  less  severe  in  its 
character. 

A  mixture  of  tannin  and  glycerin  has  a  similar  effect. 

I^. — Tannin 3i  or  oij 

Glycerin f5J. 

Mix  in  a  warm  mortar. 

Carbolic  acid  in  concentrated  form  may  be  applied  to  any  cavity. 
Jenkins,  of  Dresden,  has  recommended  that  it  be  used  hot;  it  is  par- 
ticularly useful  for  cavities  containing  masses  of  softened  dentine. 
A  variation  consists  in  the  application  to  the  cavity,  upon  a  pellet  of 
cotton,  and  heating  it  with  a  hot  burnisher. 

Sodium  bicarbonate  is  at  times  an  efficacious  remedy,  and  may  be 
freely  applied  to  the  moist  cavity. 

A  20  per  cent,  solution  of  ammonium  carbonate,  applied  for  five 
minutes  or  longer,  is  useful.^ 

The  nitrate  of  silver  powerfully  coagulates  fibrillar  protoplasm,  and 
is  useful  in  posterior  teeth  well  out  of  view  and  to  which  the  rubber 
dam  cannot  well  be  applied.  It  is  also  useful  about  undecayed  hyper- 
sensitive necks  of  molar  teeth.  It  discolors  the  dentine,  metallic  silver 
being  deposited.  For  this  reason  its  use  is  ordinarily  confined  to  pos- 
terior teeth,  though  in  some  obstinate  cases  of  hypersensitive  necks  of 
lower  incisors  and  cuspids  it  may  be  used.  To  prevent  the  production 
of  hypersensitivity  in  teeth  ground  for  bridge-work,  it  should  be 
applied  over  the  entire  crown.  It  may  be  used  in  saturated  aqueous 
.solution  upon  the  dried  dentine,  or  the  crystal  rubbed  upon  the 
slightly  moistened  dentine. 

Craven's  method  consists  of  taking  up  a  few  crystals  upon  a  hot 
platinum  wire  and  then  fusing  them  into  a  button  upon  its  roughened 
end.     This  is  then  rubbed  upon  the  dentine. 

Thiesing,  Dental  Cosmos,  November,  1903. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     371 

Miller  has  shown  that  the  silver  deposit  lessens  the  penetration  of 
acid  decalcification  (Fig.  328). 

The  subsequent  use  of  sodium  chloride  assists  in  partially  removing 
the  stains,  argentic  chloride  being  formed. 

Register  has  suggested  the  use  of  iodine  followed  by  ammonia  for 
this  purpose. 

Coming  into  contact  with  an  amalgam  filling,  or  a  bit  of  amalgam, 
an  intensely  black  deposit  is  instantly  produced,  which,  while  acid  at 
first,  is  useful  in  slowly  obtunding  dentine  in  cavities  out  of  view. 

For  severe  cases  not  yielding  to  local  treatment  at  the  time  desired, 
the  following  have  been  recommended:^ 

I^. — Trinxymethelene, 

Orthoform a  a 

Make  into  a  paste  with  carbolic  acid. 

Or, 

I^. —  Menthol  crystals 5  parts 

Phenol  crystals 4  parts 

Reduce  to  a  syrupy  liquid  to  be  used  in  place  of  the  carbolic  acid  in  the  above  formula. 

These  pastes  are  a})plied  to  the  cavity  walls  over  even  decayed 
dentine  covered  with  a  pellet  of  cotton,  and  sealed  in  with  temporary 

Fig.  328 


Dentine  treated  witli   silver  nitrate  at  a  only;   the  entire  surface  subjected  to  acid 
action  .shows  penetration  at  b.      (Miller.) 

stopping  for  twenty-four  hours  only.  Formaldehyde  gas  is  liberated 
in  the  nascent  state  and  desensitizes  the  fibrils  by  hardening  and 
fixing  them  as  in  histological  specimens. 

In  shallow  cavities  and  upon  abraded  surfaces  nitric  and  chromic 
acid  accurately  applied  in  small  quantity  upon  a  gold  probe  is  useful. 
Any  softened  dentine  must  later  be  reniovt^d  and  filled. 

Aside  from  the  treatment  of  hyj)ersensitive  dentine,  at  the  time  of 

'  G.  Mahe,  M.D.,  Paris,  Dental  Co.smos,  1904. 


372  DENTAL  CARIES 

operation,  analgesics  may  be  introduced  for  their  power  of  gradually 
lessening  the  hyperirritability  of  fibrillar  protoplasm.  If  cotton  wedges 
are  introduced,  antiseptic  analgesics,  particularly  oil  of  cloves,  equal 
parts  of  oil  of  cloves  and  carbolic  acid,  and  phenol  camphor,  may  be 
used  on  the  cotton  with  advantage. 

A  partially  prepared  cavity  may  be  moistened  with  oil  of  eucalyptus 
and  temporarily  filled  with  temporary  stopping  or  gutta-percha. 

A  temporary  filling  made  by  mixing  zinc  oxide  with  Fletcher's 
carbolized  resin  or  eugenol  to  a  stiff  paste  will  endure  for  some  time, 
and  reduce  hypersensitivity.  It  is  also  useful  as  an  antiseptic  sedative 
test  filling. 

J^. — Carbolic  acid, 

Colophony aa      Bj 

Chloroform fSss— M.     (Fletcher.) 

The  use  of  chalk  applied  nightly  in  a  superficial  cavity,  as  at  the 
cervix,  is  useful  for  this  purpose. 

In  cases  in  which  devitalization  is  intended,  arsenic  may  be  used 
as  an  obtundent  to  effect  a  deeper  placing  of  another  portion  as  a 
devitalizing  agent;  twenty-four  to  forty-eight  hours  are  required  for 
this  purpose.  If  left  long  enough  it  will  devitalize  the  pulp  even 
through  a  large  mass  of  dentine. 

There  is  no  safety  in  short  applications  as  a  means  of  obtunding 
dentinal  hypersensitivity.  The  pulp  may  die  even  after  seeming 
excavation  of  all  affected  dentine. 

Ninety  per  cent,  of  cavities  may  be  comfortably  excavated  with 
sharp  instruments  by  the  aid  of  dryness  and  carbolic  acid.  A  small 
percentage  require  the  use  of  caustics,  etc.,  while  in  a  still  smaller 
number  cataphoresis  is  the  only  certain  remedy.  / 

During  seasons  in  which  acid  fruits  are  consumed,  much  hyper- 
sensitivity may  be  induced.  This  should  always  lead  to  examination 
for  cavities  of  decay,  but  such  may  not  exist  or  may  be  properly  filled. 

For  hypersensitivity  about  undecayed  necks  of  teeth,  the  mouth 
should  be  kept  in  an  alkaline  condition  by  means  of  dilute  plieuol 
sodiqiie  or  sodium  bicarbonate,  or,  better,  by  the  use  of  more  lasting 
mild  alkalies,  such  as  chalk,  or  milk  of  magnesia,  or  a  combination  of 
the  two.  The  manufacturers  of  milk  of  magnesia  recommend  a  series 
of  oil  mixtures;  6  drops  of  any  mixture  to  be  shaken  up  with  the 
contents  of  the  original  bottle  as  a  flavor  to  remove  the  naturally  raw 
taste  of  the  preparation,  which  is  disagreeable  to  some  persons.^  The 
following  are  two  of  the  simplest: 

'  Items  of  Interest,  1905,  p.  977. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS     373 

I^.— Oil  of  bitter  almond 1  part 

Oil  of  anise 3  parts 

Or, 

I^. — Oil  of  cinnamon 3  parts 

Oil  of  wintergreen 4  parts 

The  use  of  potassium  carbonate  in  n-lvc-eriii  is  indicated  and  may 
be  given  to  the  patient  for  free  use. 

For  hypersensitive  incisal  edges  or  occhisal  surfaces  Robinson's 
remedy  may  be  thus  dispensed  with  a  caution  as  to  its  caustic 
nature. 

At  times  zinc  chloride,  Robinson's  remedy,  and  silver  nitrate  must 
be  used  by  the  ojx'rator.  For  very  obstinate  cases  of  cervical  hy})er- 
sensitivity  Flagg  recommended  the  use  of  the  electric  cautery,  the 
spots  to  be  seared.     A  very  hot  burnisher  may  occasionally  serve. 

In  a  number  of  the  localized  cases  fillings  may  be  subsecjuently 
required  unless  rigid  prophylaxis  be  practised.  Acid  mouth  v^ashes 
should  be  avoided.  Prophylaxis  may  remove  the  superficial  desensi- 
tized layer,  and  the  application  re(|uire  renewal. 


CHAPTER   XIV. 

DENTAL  CARIES:    THERAPEUTICS  AND  PROPHYLAXIS. 

According  to  the  depth  of  invasion  and  variations  in  the  thera- 
peutics involved,  caries  may  be  divided  into  eight  stages,  as  follows: 

1.  Superficial  caries,  or  that  stage  in  which  the  enamel  has  been 
partially  decalcified,  but  the  dentine  not  affected. 

2.  Simple  caries,  in  which  the  dentine  has  been  affected  slightly 
in  such  a  manner  as  ordinarily  to  compel  the  formation  of  a  cavity 
and  its  filling. 

3.  Deep-seated  caries,  in  which  the  complete  excavation  of  the 
cavity  renders  pulp  injury  a  possibility,  but  the  pulp  is  not  very 
dangerously  approached. 

4.  Almost  exposed  pulp.  This  is  a  refinement  of  the  preceding 
stage,  in  which  pulp  exposure  becomes  an  imminent  danger  during 
excavation  of  the  cavity  and  special  therapeutics  are  demanded. 

5.  Exposed  pulp,  in  which  the  actual  exposure  of  the  pulp  by 
decay  or  by  accident  or  intention  during  excavation  renders  its  treat- 
ment necessary,  or  in  which  disease  of  the  pulp  compels  canal  treat- 
ment. 

6.  Perforation  by  caries,  in  which  after  pulp  death  secondary  caries 
of  dentine  and  cementum  has  caused  an  opening  into  the  pericemental 
tract. 

7.  Loss  of  crown  by  caries. 

8.  Loss  of  root  by  caries. 

Each  of  these  stages  of  caries  requires  special  consideration  and  a 
therapeutics  adapted  to  each. 

THERAPEUTICS  OF  SUPERFICIAL  CARIES. 

About  cavity  margins,  beneath  green  stain,  etc.,  and  at  points  of 
approximal  contact  of  teeth  may  frequently  be  seen  areas  of  enamel 
(Icculcification,  the  enamel  not  being  entirely  penetrated  (Fig.  291). 

It  is  possible  at  times  to  remove  the  decalcified  portion  by  means 
of  c'ar})f)riindum  strips,  files,  or  disks.  If  the  surface  be  highly 
polished   by  means  of  pumice  and  chalk,  and  subsequent  prophy- 


THERAPEUTICS  OF  SIMPLE  CARIES  375 

laxis  be  employed,  the  practice  may  be  endorsed  for  the  better  grades 
of  teeth,  and  particularly  in  the  anterior  part  of  the  mouth.  As  a 
rule,  however,  the  attempt  to  remove  supposed  superficial  enamel 
caries  demonstrates  the  fact  that  the  enamel  is  deeply  affected,  and  in 
all  probability  the  dentine  as  well.  The  attempt  to  remove  such 
caries  upon  proximal  surfaces  by  files  and  stones  results  in  tooth 
deformity,  the  exposure  of  dentine  to  the  fluids  of  the  mouth,  and  the 
destruction  of  the  contact  points,  except,  perhaps,  when  in  the  anterior 
teeth  a  lingual  approach  is  made.  It  is  sometimes  proper  to  remove 
the  slight  superficial  caries  found  about  a  cavity,  either  prior  to 
excavation  in  order  to  determine  the  real  cavity  boundary,  or  after 
excavation  if  such  removal  would  give  an  even  better  tooth  form  and 
lessen  a  recurrence  of  decay,  or,  in  some  cases,  after  filling  when 
both  filling  and  margin  are  reduced  together  to  a  proper  form  and 
integrity  of  enamel.  Some  judgment  is  required  in  such  a  matter, 
and  no  enamel  should  be  so  treated  if  any  doubt  exist  as  to  its  future 
integrity,  but  the  cavity  should  rather  be  extended  to  include  the 
doubtfid  area. 

It  may  be  considered  a  safe  rule  to  examine,  by  means  of  the  electric 
mouth  lamp,  any  cases  of  suspected  superficial  caries  in  order  to  deter- 
mine the  depth  of  enamel  invasion. 

The  large  majority  of  such  cases,  especially  in  the  poorer  grades 
of  teeth,  will  l)e  found  to  be  of  the  class  called  here  simple  caries. 

Upon  the  labial  or  buccal  surfaces  of  anterior  teeth  a  superficial 
decalcification  may  be  found.  This  may  be  removed  by  abrasives, 
the  surface  highly  polished,  and  the  patient  enjoined  to  use  great  care 
in  prophylaxis.  Any  spots  at  which  simple  caries  exists  should  be 
excavated  and  filled. 

There  is  also,  at  times,  a  slight  superficial  decalcification  about 
simple  approximal  cavities,  and  its  removal  would  leave  the  slightly 
disked  margin  wall  free  from  contact  with  the  adjoining  tooth. 
Such  a  removal  is  at  times  warrantable,  either  before  or,  at  times, 
after  filling.  A  superficial  caries  of  cementum  and  dentine  may  exist. 
This  may  be  removed,  the  dentine  polished,  and  nitrate  of  silver 
applied  if  the  surfaces  be  not  exposed  to  view. 


THERAPEUTICS  OF  SIMPLE  CARIES. 

The  cases  cited  above  and  all  detectable  cavities  of  very  limited 
depth  may  be  classed  as  cases  of  simple  caries.     The  teeth  should  be 


376  DENTAL  CARIES 

wedged  apart  if  this  be  needed  for  access,  all  decalcified  enamel  and 
dentine  removed,  the  cavity  properly  extended  and  shaped,  and,  as 
a  rule,  a  filling  of  gold  inserted.  All  fissures  about  a  cavity  should  be 
freely  opened  to  their  extremities  and  made  a  part  of  the  general  cavity. 

The  extension  upon  approximal  surfaces  should  include  all  super- 
ficial decay  that  cannot  be  so  disked  oft'  as  to  bring  the  filling  margin 
into  the  embrasures. 

At  times,  expediency — i.  e.,  the  systemic  condition  of  the  patient, 
the  character  of  the  decay  or  of  the  surrounding  tooth  structure,  or 
economy — warrants  the  use  of  a  good  amalgam  where  resistance  to 
attrition  is  required,  or  occasionally  of  gutta-percha,  in  suitable 
locations  not  exposed  to  attrition.  Upon  the  labial  surfaces  of 
incisors  porcelain  inlays  combine  efficiency  with  esthetics. 

If  a  simple  cavity  prove  inordinately  sensitive,  the  more  powerful 
remedies  may  be  freely  used  to  reduce  the  hypersensitivity,  and  the 
cavity  should  be  treated  with  carbolic  acid  before  filling,  particularly 
when  gold  is  to  be  used  in  cervicolabial  cavities  of  incisors.  By  this 
means  the  subsequent  effect  of  thermal  changes  is  lessened.  Recur- 
rence of  caries  is  more  likely  about  small  fillings  because  the  original 
condition  may  recur,  but  they  are  often  a  necessity.  Subsequent 
prophylaxis  is  of  importance,  and  to  that  end  all  fillings  should  be 
made  as  smooth  and  perfect  as  possible. 

THERAPEUTICS  OF  DEEP-SEATED  CARIES. 

In  this  stage  of  caries  there  is  usually,  although  by  no  means  always, 
an  easily  discoverable  cavity  of  size.  After  the  removal  of  ragged  and 
overhanging  enamel  margins,  and  of  loose  debris  in  the  cavity,  it  is 
noted  that  the  response  to  thermal  impulse  is  painful  and  prompt.  In 
washing  such  cavities,  water  at  a  temperature  of  about  100°  F.  should 
always  be  used;  cold  or  very  hot  water  being  only  employed  in  cavity 
irrigation  to  test  the  promptitude  of  response  upon  the  part  of  the 

pulp- 
In  treating  hypersensitivity  of  dentine  carbolic  acid  is  to  be  pre- 
ferred, the  mineral  acids  are  avoided,  and  if  strong  agents  like  zinc 
chloride  or  Robinson's  remedy  are  used,  the  cavity  floor  is  to  be 
varnished  with  chloropercha  or  ''cavitine"  varnish,  which  are  imper- 
meable. If  necessary,  essential  oils  or  a  saturated  solution  of  cocaine 
in  glycerin,  thymol  in  alcohol,  or  menthol  in  chloroform  may  be  sealed 
in  for  twenty-four  hours. 


THERAPEUTICS  OF  DEEP-SEATED  CARIES  377 

A  mixture  of  cocaine  with  nervocidine  may  be  useful,  as  indicated 
by  Soderberg.     (See  pages  371  and  372). 

Cocaine  cataphoresis  is  regarded  as  admissible  in  all  stages  of  caries. 

The  removal  of  all  the  softened  dentine,  which  should  be  done  in 
these  cases,  forms  a  cavity  of  such  magnitude  that  proximity  to  the 
pulp  is  evident.  The  softening  has  proceeded  for  a  distance  beneath 
the  enamel,  so  that  when  all  softened  dentine  is  cut  away  from  beneath 
it  the  latter  tissue  may  overhang  the  general  cavity  unsupported. 
These  overhanging  walls  are  cut  away  until  the  region  of  strong 
enamel  is  reached,  and  then  it  may  be  that  the  walls  still  over- 
hang the  general  cavity.  It  is  usually  not  necessary  nor  advisable  to 
remove  this  portion  of  enamel. 

At  the  completion  of  excavation  the  pulpal  wall  of  the  cavity  will 
be  in  fair  proximity  to  the  pulp.  A  blast  of  cool  air  from  a  chip 
syringe  may  produce  an  immediate  response  upon  the  part  of  the 
pulp,  vigorous  in  proportion  to  the  thinness  of  its  dentinal  covering 
and  its  irritability. 

In  many  cases  non-conducting  substances  are  required  as  inter- 
mediates between  the  pulpal  wall  and  the  metal  filling.  In  many 
other  cases  the  metal  filling  may  be  placed  directly  upon  the  dentine 
without  danger.  In  some  cases  a  simple  layer  of  non-conducting  var- 
nish, such  as  "cavitine,"  will  be  sufficient.  In  others  zinc  phosphate 
or  gutta-percha  must  be  added.  The  degree  of  the  response  to  a  blast 
of  cool  air  will  afford  a  guide  to  the  nature  of  the  intermediate  required 
if  any  be  deemed  necessary.  In  no  case  should  varnish  or  gutta- 
percha be  allowed  to  remain  in  the  portions  of  cavity  that  support 
the  covering  filling  material  and  which  is  subjected  to  the  force  of 
mastication.  The  resilient  nature  of  such  substances  will  cause  the 
loosening  of  the  filling  and  probably  induce  mechanical  or  infective 
irritation  of  the  fibrils  and  through  them  of  the  pulp. 

In  some  cases  the  undermined  state  of  the  enamel  wall  necessitates 
the  use  of  an  adhesive  zinc  phosphate  as  a  means  of  support  by  re- 
placing the  lost  dentine,  and  in  such  the  pulpal  wall  may  be  covered 
and  so  protected  from  impact  as  well  as  from  thermal  changes. 

The  action  of  zinc  phosphate  upon  dentinal  fibrils  and  the  pulp 
being  a  matter  of  some  doubt,  it  is  better  that  the  pulpal  wall  be 
varnished  before  it  is  introduced.  The  varnish  not  only  acts  as  an 
impervious  coating,  but  also  serves  as  an  additional  non-conductor. 
If  made  antiseptic  it  is  still  more  useful. 

After  the  cavity  is  prepared  it  is  sterilized  and  dried,  as  described 


378  DENTAL  CARIES 

in  the  next  stage  of  caries,  is  coated  with  "cavitine"  varnish,  and 
Harvard  zinc  phosphate  mixed  stiff  is  packed  into  the  undercuts  and 
over  the  pulpal  wall. 

When  set  the  enamel  margins  are  freed  of  cement  and  the  cement 
is  excavated  to  the  form  required.  In  some  cases  cement  can  only 
be  placed  over  the  pulpal  wall,  owing  to  lack  of  room  for  both  cement 
and  the  covering  filling.  In  such  cases  the  combined  use  of  soft 
cement  and  gold,  or  soft  cement  and  amalgam,  is  useful. 

In  deep-seated  caries  the  extension  of  cavity  margins  in  such  a 
manner  as  to  prevent  recurrence  of  decay  is  demanded.  Upon  approx- 
imal  surfaces  the  ideal  conditions  are  an  extension  of  buccal  and 
lingual  margins  to  a  point  which  will  permit  a  contoured  metal  filling 
to  have  its  corresponding  buccal  and  lingual  margins  well  irrigated 
by  the  action  of  the  tooth-brush  and  food  in  mastication.  Often 
a  slight  alteration  of  tooth  form,  together  with  contouring  of  fillings, 
accomplishes  the  end  desired  without  undue  cutting  of  tooth  structure. 
Thus,  the  cervical  margin  may  be  slightly  reduced  with  strips  or  disks 
to  assume  an  absence  of  contact,  but  the  enamel  must  not  be  totally 
removed.  The  lingual  or  buccal  margin  may  be  treated  in  a  similar 
manner. 

The  cervical  margin  of  the  cavity  and  filling  are  best  protected  when 
overlapped  by  healthy  gum  tissue,  and,  if  possible,  should  be  so 
arranged.  The  cervical  margin  should  always  be  extended  beyond 
the  contact  point  in  such  cases,  whether  carried  beneath  the  gum  or 
not.     Incisal  margins  are  to  have  similar  consideration. 

Firm  approximal  contact  of  fillings  or  filling  and  tooth  are  required 
to  prevent  packing  of  food  into  the  interproximal  space.  This  would 
both  injure  the  gum  and  introduce  the  fermentable  element  in  caries 
production.  The  point  of  contact  should  be  neatly  rounded  to 
produce  a  normal  contact.  This  contact  should  be  obtained  even  if 
the  filling  must  be  overcontoured. 

An  exception  may  at  times  be  made  where  a  space  has  previously 
naturally  existed  and  the  gum  margin  is  healthy. 

Teeth  sliould  never  be  joined  by  fillings  alone,  as  one  or  both  will 
usually  loosen.  If  necessary  for  the  protection  of  the  gum,  both  may 
be  crowned  and  the  crowns  united  by  solder,  or  a  staple  may  be  placed 
in  the  pulp  canals  of  the  two  teeth.  About  this  a  common  filling  may 
be  built.  It  may  be  that  gold  inlays,  locked  in  spacious  "doll  heads"  or 
the  occlusal  .surfaces  of  both  teeth,  and  extending  over  to  opposite 
approximal  surfaces  as  well  as  into  the  cavities,  may  l)e  joined  or  cast 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP  379 

double  as  a  means  of  support.      The  strain  upon  such  fiUings  is 
very  great  when  occlusion  exists.     (See  Pyorrhea  Alveolaris.) 


THERAPEUTICS  OF   ALMOST  EXPOSED   PULP. 

In  this  stage  of  caries  complaint  is  usually  made  that  for  some 
time  pain  has  been  produced  by  the  presence  in  the  mouth  of  cool 
or  hot  substances.  Several  classes  of  almost  exposed  pulps  may  be  . 
discovered  after  opening  the  cavity  and  removing  the  bulk  of  the 
decayed  dentine.  In  the  simplest  class  the  pulpal  wall  may  be  found 
sound  after  removal  of  all  decalcified  dentine.  This  makes  practically 
a  case  of  deep-seated  caries  and  is  to  be  treated  as  such,  the  close 
approach  to  the  pulp  simply  demanding  additional  precautions  as 
to  non-conduction,  prevention  of  compression,  and  infection.  The 
cavity  is  to  be  sterilized  with  1  per  cent,  formaldehyde,  5  per  cent, 
sodium  dioxide  solution,  etc.,  and  dried;  over  the  jnd])al  wall  "cavi- 
tine"  with  hydronaphthol  added  is  painted  and  dried: 

I^. — Hydronaphthol gr.  ij 

Alcohol gtt.  XX — M. 

Add  to  the  half-ounce  bottle  of  "cavitine."' 

A  thin  wafer  of  softened  gutta-pt^rcha  is  to  be  laid  over  the  ])ulpal  wall 
in  such  manner  as  not  to  interfere  with  the  introduction  of  cement. 
Harvard  zinc  phosphate  mixed  to  a  consistency  just  suited  to  the  case 
may  be  pressed  laterally  into  the  undercuts  and  will  spread  nicely 
over  the  gutta-percha  without  pressure.  Under  no  circumstances 
must  the  superstructures  depend  ii])on  the  gutta-percha  base  as  a 
support,  as  the  filling  may  loosen  or  the  wall  be  broken. 

The  operation  may  be  varied  for  cases  of  but  limited  retaining 
periphery  by  gently  spreading  the  zinc  phosphate  over  the  varnish, 
or,  in  some  cases,  the  gold  and  zinc  phosphate  or  amalgam  and  zinc 
phosphate  combination  may  be  required. 

In  the  use  of  gold  and  zinc  phosphate  a  portion  of  crystal  gold  is 
gently  tapped  into  a  mass  of  soft,  quick-setting  cement  placed  over  the 
varnish  and  the  setting  of  the  cement  awaited.  The  gold  is  then 
condensed  and  more  added. 

With  the  amalgam  and  zinc  phosphate  combination,  ixiivv  placing 
the  gutta-percha,  soft  cement  is  j)laced  u])()n  one  cavity  margin  and 

'"Cavitine,"  or  "crystalline"  of  commerce,  is  composed  of  trinitrocellulose  dissolved  m 
subacetate  of  amyl 


380  DENTAL  CARIES 

a  ball  of  previously  prepared  amalgam  is  laid  upon  it.  Pressure  upon 
the  amalgam  by  means  of  a  ball  burnisher  causes  the  cement  to  be 
spread  over  the  cavity  wall  in  advance  of  the  amalgam.  It  practically 
inlays  the  metal  filling,  but  permits  a  better  marginal  joint  with  the 
metal.  The  margins  are  freed  of  amalgam  and  cement,  and  the  opera- 
tion is  completed  with  amalgam.  It  also  prevents  the  shifting  and 
dislodgement  in  any  degree  of  the  metal  filling  which  sometimes 
occurs  in  the  act  of  introduction,  unless  guarded  against. 

This,  of  course,  refers  to  locations  in  which  the  latter  is  indicated. 
The  cement  in  the  combination  increases  the  adhesion  and  prevents 
leakage  and  the  discoloration  of  the  walls  by  the  amalgam.  A  trifle 
of  aristol  or  hydronaphthol  added  to  the  cement  (1  to  10)  imparts  to 
it  an  antiseptic  character  without  impairing  its  integrity  as  a  cement. 
Neither  should  be  used  in  connection  with  thin  enamel  walls  exposed 
to  view. 

The  second  class  of  almost  exposed  pulp  is  that  in  which  thorough 
excavation  would  cause  exposure  of  the  pulp. 

If  the  dentine  be  of  the  disintegrated,  boggy  sort,  it  should  be 
removed  regardless  of  exposure;  but  if  it  be  simply  softened  by 
decalcification  and  be  quite  firmly  adherent  to  the  cavity  floor,  and 
particularly  if  it  be  somewhat  thickly  distributed,  the  deeper  layers 
may  be  left  in  situ,  as  a  pulp  covering. 

In  such  cases  all  lateral  walls  should  be  thoroughly  excavated  and 
only  a  thin  layer  left  over  the  pulp  horns.  While,  without  doubt,  the 
tubules  of  decalcified  dentine  are  liable  to  be  invaded  by  bacteria, 
Miller  has  shown  that  frequently  such  dentine  may  exist  without 
invasion.    (See  Fig.  309.) 

The  argument  that  such  dentine  contains  poisonous  products  of 
bacteria  deleterious  to  the  pulp  does  not  seem  borne  out  by  results 
in  carefully  handled  cases. 

That  .some  of  these  protected  pulps  may  die  is  a  fact  not  to  be 
disputed,  but  that  many  live  in  security  is  also  true.  Whether  such 
dentine  can  be  recalcified  has  not  jet  been  scientifically  sliown,  but  cer- 
tain cases  treated  with  oxychloride  of  zinc  have  shown  evidences  of 
it,  and  Miller  records  cases  of  hardening  of  such  caries  even  without 
treatment. 

The  treatment  required  for  this  dentine  is:  (1)  neutralization  of  the 
acid  present;  (2)  .saturation  with  a  permanent  antisej^tic;  (3)  an 
antiseptic  non-conductive  covering. 

After  drying,  a  weak  solution  of  sodium  bicarbonate  or  ammonium 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP  381 

hydrate  will  accomplish  the  first  requirements.  The  dentine  is  then 
thoroughly  dried  and  saturated  with  "cavitine"  varnish  containing 
hydronaphthol  or  a  solution  of  ('aiuida  balsam  containing  hydro- 
naphthol,  or  thin  chloropercha  containing  aristol  or  iodoform,  or 
the  formaldehyde  jircparations  known  as  "Formagen"  and  "Jodo- 
Formagen"  may  be  spread  over  it,  or  oxychloride  of  zinc,  the  fluid 
of  which  has  been  diluted  one-third  with  water,  may  be  used  as  a 
covering.     (Use  fluid,  2  drops;  distilled  water,  1  drop.) 

Williams^  suggests  that  the  decalcified  dentine  be  first  saturated 
with  absolute  alcohol  for  one  minute,  then  dried,  then  wet  with  oil 
of  cloves  for  one  minute,  then  again  dried,  after  which  the  varnish, 
etc.,  is  to  be  used.  Solution  of  sulphate  of  copper  may  be  used  to 
saturate  the  dentine,  after  which  it  should  be  dried  and  encased  in 
varnish. 

The  use  of  these  preparations  obviates  the  necessity  of  sealing 
temporary  antiseptics  in  the  cavity,  as  they  are  in  themselves  more 
or  less  permanently  antiseptic.  Over  them  asbestos  paper  or  thin 
gutta-percha  is  placed,  and  then  zinc  phosphate,  made  antiseptic  with 
aristol  or  hydronaphthol,  is  packed,  and  if  any  doubt  exist,  the  cavity 
is  temporarily  sealed  with  gutta-percha  or  temporary  stopping,  ^^"hen 
all  doubt  is  at  rest  the  metal  filling  may  be  placed.  In  another  method, 
useful  in  doubtful  cases  in  determining  the  possible  bad  reaction  of  the 
j)idp,a  (juite  stiffly  mixed  paste  of  eugenol  and  Hubbuck's  zinc  oxide 
may  be  introduced  into  the  floor  of  the  cavity,  gently  pressed  to  place 
with  cotton,  and  covered  with  sandarac  or  cotton.  It  hardens  after  a 
few  hours;  at  a  subsequent  sitting  part  of  it  may  be  left  as  a  reason- 
ably firm  antiseptic  foundation.  If  desired,  the  entire  cavity  may  be 
filled  with  it,  or,  better,  to  a  slightly  concave  surface.  Exposed  to 
the  saliva  it  hardens  to  a  degree  sufficient  to  act  as  a  cement  tempo- 
rary filling  for  weeks  or  months,  or,  occasionally,  even  years.' 

In  some  cases  of  deep-seated  caries  in  which  gold  filling  is  desirable, 
but  in  which  linings  are  contra-indicated,  yet  in  which  immediate 
filling  with  metal  would  involve  such  thorough  excavation  as  to 
endanger  pulp  vitality  either  as  the  result  of  excavation  or  subsequent 
thermal  shocks,  oxychloride  of  zinc  may  be  placed  in  the  perij)hcrally 
prepared  cavities  and  over  considerable  masses  of  decalcified  dentine. 
If  allowed  to  remain  for  several  months  (three  to  six)  the  oxychloride 
stinmlates  the  pulp  to  the  formation  of  some  secondary  dentine,  and 
complete  excavation  to  a  sound  basis  may  be  made.     There  is  also 

J  Items  of  Interest,  1898.  •  -  Dr.  t>.  Blair  Luckie. 


382  DENTAL  CARIES 

some  evidence  of  hardening  of  the  dentine.  This  method  is  open 
to  the  possible  objection  that  secondary  dentine  is  a  source  of  future 
trouble,  but  the  method  has  its  advantages  in  badly  decayed  anterior 
teeth. ^  In  very  deep  cavities  the  fluid  of  the  oxychloride  should  be 
diluted  one-third  with  distilled  water  for  the  first  portion. 

In  these  cases  porcelain  inlays,  with  their  underlying  cement,  should 
have  due  consideration  as  therapeutic  means. 

In  deep  and  very  deep-seated  caries,  in  situations  in  which  discolor- 
ation is  not  of  great  moment,  the  cavity  may  first  be  lined  with  copper 
amalgam  for  its  antiseptic  value.  This  is  advanced  toward  setting 
by  the  use  of  a  wafer  of  amalgam  from  which  the  mercury  has  been 
expressed.  The  filling  material  is  then  dished  out  so  that  the  cavity 
margins  are  freed  of  it.  The  ordinary  amalgam  is  then  added  to 
contour.  Copper  amalgam  alone  ordinarily  becomes  disintegrated 
and  caries  recurs.  Occasionally  it  lasts  well  (especially  Sullivan's) ; 
copper  and  its  salts  are  germicidal  in  a  short  time.  The  ordinarily  good 
behavior  of  somewhat  doubtful  dentine  under  it  is  thus  explained. 

Dobrzyniecki^  (Budapest),  in  eight  experimental  cases  upon  micro- 
scopically sound-looking  dentine,  claims  to  have  found  the  Bacillus 
gangrense  pulpse  vital  after  months  of  enclosure  under  sealed  dress- 
ings of  camphor,  concentrated  carbolic  acid,  or  eucalpytus  oil.  All 
other  organisms  were  devitalized.  As  Arkovy's^  experiments  showed 
the  decided  influence  of  carbolic  acid  over  this  organism,  and  as  root- 
canal  antiseptics  are  nearly  always  successful  in  cases  of  moist  gan- 
grene of  the  pulp  (Bacillus  gangrense  pulpse  Arkovy),  the  difficulty  of 
destroying  this  germ  by  germicides  left  indefinitely  in  the  cavity  must 
be  accepted  with  reservation. 

In  some  desperate  cases  with  the  walls  frail  the  cements,  either  zinc 
phosphate  or  Ascher's  artificial  enamel,  or  similar  so-called  silicate 
cements,  may  be  used  as  a  last  resort  before  crowning.  The  silicate 
cements  are  less  soluble  in  the  acids  contained  in  saliva  or  formed 
from  carbohydrates  against  the  filling  than  are  the  zinc  phosphates. 

Ilinkins  and  Acree*  claim  that  one-fifth  of  1  per  cent,  is  sufficient 
to  dissolve  the  zinc  phosphate,  and  that  enough  acid  elements  enter 
from  the  blood  to  aft'ect  it. 

'  In  some  ca.ses  of  this  sort  seen  by  tlie  writer,  and  observed  for  from  ten  to  sixteen  years, 
tlie  ill  results  of  oxychloride  of  zinc  claimed  have  not  been  observed.  In  one  case,  after  six- 
teen years,  a  lateral  incisor  crown  broke  off,  and  the  pulp  was  found  to  have  receded,  but  was 
otherwise  apparently  healthy.  The  question  i,s  one  of  the  advisability  of  immediate  devitaliza- 
tion, with  it.s  advantages  and  disadvantages  in  anterior  teeth,  or  of  a  possible  remote  pulp 
death,  etc. 

2  Soderberg  upon  Arkovy,  Dental  (>)smr)s,  1899.  '  Ibid. 

*  See  Dental  Cosmos,  .June,  1901,  and  March,  190.5. 


THERAPEUTICS  OF  EXPOSED  PULP  383 

The  silicate  cements  dissolve  more  readily  under  friction  than  under 
the  action  of  acid,  so  that  of  two  fillings  the  one  which  is  not  exposed 
to  attrition  or  brush  action  is  usually  in  better  condition  after  about  two 
years. 

THERAPEUTICS  OF   EXPOSED   PULP. 

The  exposure  of  the  pulp  may  be  the  direct  result  of  caries;  the 
removal  of  boggy,  disintegrated  dentine  may  produce  it,  or  it  may 
be  the  result  of  the  removal  of  a  last  layer  of  decalcified  dentine  or 
of  the  careless  or  inadvertent  perforation  of  sound  dentine  by  instru- 
ments. Fracture  or  abrasion  are  occasionally  responsible  for  exposure. 
Erosion  rarely  causes  it. 

Diagnosis. — After  excavation  of  the  cavity,  washing  with  tepid  water, 
and  drying,  direct  vision  or  a  reflected  image  in  the  mouth-mirror 
may  reveal  the  area  of  exposure  as  a  round  opening  occupied  by  a 
pinkish  or  red  body.  If  the  exposure  be  reasonably  large,  pulsation  of 
the  red  body  may  usually  be  observed.  The  exposure  may  be  so 
slight  as  to  be  invisible,  the  depth  of  the  cavity,  however,  indicating 
that  exposure  probably  exists.  Bleeding  is  a  certain  guide,  but 
bleetling  from  the  gum  margin  must  be  borne  in  mind.  Truman 
advises  in  these  cases  that  finely  carded  cotton  be  gently  passed  over 
the  cavity  w^alls,  exposure  being  detected  by  the  momentary  pain 
produced  when  the  fibers  pass  over  the  area  of  exposure. 

As  this  test  may  fail,  in  cases  of  known  exposure,  it  is  not  altogether 
reliable,  but  is  fairly  so  when  pain  is  produced. 

A  finely  pointed  j)r()be  may  be  gently  dragged  over  the  pulpal  wall 
and  catches  in  the  orifice  of  exposure,  however  small.  A  slight,  quick 
start  upon  the  part  of  the  patient  is  usually  elicited.  This  may  consist 
simply  of  a  winking  of  the  eyelid.  Flagg  warned  against  requesting 
an  affirmative  nod  by  the  patient,  as  this  would  cause  injury  to  the 
pulp.  Delicately  used,  this  test  is  the  most  reliable  in  all  classes  of 
cases,  and  is  not  painful. 

It  is  to  be  remembered  that  disease  may  have  caused  a  loss  of  a 
portion  of  a  pulp  horn,  in  which  case  the  cotton  test  will  fail;  gentle 
exploration  will  detect  the  amount  lost.  Blood,  or  pus  followed  by 
blood,  are  evidences  of  exposure. 

Excruciating  pain  following  mastication,  or  pressure  or  suction 
exerted  upon  the  cavity  by  means  of  the  tongue,  are  subjective  symp- 
toms indicating  a  probable  diagnosis  of  exposure.    Exacerbation  of 


3S4  DENTAL  CARIES 

throbbing  pain  following  the  use  of  salt,  sweet,  or  acid  foods  are  fairly 
indicative  of  a  practical  exposure. 

Treatment. — ^An  exposed  pulp  is  either  to  be  capped  or  removed  and 
the  canals  filled. 

The  consensus  of  opinion  is  that  ordinarily  all  pulps  should  be 
removed,  except  those  freshly  exposed  by  removal  of  simply  decalcified 
dentine  and  by  accident.  There  is  no  certainty  that  pulps  exposed 
by  caries  or  practically  so  will  live  under  capping  materials,  but  the 
attempt  may  be  made  at  times  for  special  reasons. 

Freshly  exposed  pulps  may  be  capped  or  removed.  Perhaps  a  good 
rule  would  confine  capping  to  anterior  teeth  of  the  better  grades  in 
patients  in  good  physical  condition,  and  to  pulps  in  teeth  having 
incomplete  roots.  The  improved  methods  of  pulp  removal  and  canal 
antisepsis  warrant  pulp  destruction  as  a  safer  method  than  capping 
in  most  posterior  teeth.  Even  in  anterior  teeth  pulp  removal  for 
anchorage  purposes,  if  needed,  is  quite  warrantable.  The  advantages 
of  capping  are  maintenance  of  tooth  translucency  and  the  avoidance 
of  canal  work. 

The  disadvantages  are:  (1)  Possible  death  of  the  pulp  by  hyper- 
emia due  to  conduction  of  thermal  changes.  (2)  An  overproduction 
of  secondary  dentine,  the  production  of  pulp  nodules,  or  other  de- 
generative changes,  the  pulp  becoming  exhausted  and  death  ensuing. 
Increased  difficulty  of  canal  treatment  may  result.  (3)  Disease  of 
the  pulp  due  to  infection  beneath  the  capping  material.  (4)  The 
time  required  for  assurance  of  success  or  failure. 

The  object  sought  in  capping  is  the  protection  of  the  pulp  from 
thermal  changes,  infection,  and  compression,  as  either  is  fatal  to  pulp 
vitality.  This  is  best  accomplished  by  placing  against  the  pulp,  or 
by  placing  in  contact  with  the  pulp,  an  antiseptic  paste  beneath  a 
metal  cap,  or  an  antiseptic  cement  having,  when  set,  sufficient  rigidity 
to  permit  other  work  to  be  done. 

Prognosis  is  favorable  for  the  cases  selected  as  suggested. 

Pulp  Capping. — The  metal  cap  should  be  made  of  platimim  or  gold 
for  anterior  teeth.  Tin,  lead,  or  silver  may  be  used  posteriorly.  After 
punching  or  trimming  to  shape  it  should  be  made  concavo-convex 
by  pressing  it  into  soft  wood  by  means  of  the  rounded  end  of  an 
instrument  handl(>.  A  film  of  wax  is  placed  on  the  convex  side; 
a  warmed,  small  l)ijrnisher  is  attached,  and  the  cap  is  adjusted  in 
proper  position  by  trying  in  the  cavity.  It  is  then  to  be  filled  with 
the  capping  material  (a  little  of  the  latter  placed  in  any  depression 


THERAPEUTICS  OF  EXPOSED  PULP  385 

at  the  point  of  exposure  in  order  to  exclude  air) ;  then  one  side  of  the 
cap  is  laid  upon  the  dentine  and  the  other  gra(hially  brought  down, 
and  the  edges  of  the  cap  firmly  adapted  to  the  dentine.  This  causes 
the  paste  to  exude  from  beneath  the  cap.  Any  excess  is  gently  re- 
moved with  an  excavator  if  not  of  an  immediately  setting  paste.  A 
little  "cavitine"  varnish  or  chloropercha  is  to  be  placed  over  the 
pulpal  wall  and  cap  and  dried.  A  little  soft  zinc  phosphate  or 
oxychloride  of  zinc  cement  is  now  placed  over  the  varnish  as  a  pro- 
tection, and  when  set  the  filling  is  completed  with  gutta-perc-ha  or 
zinc  phosphate  cement,  which  is  to  be  allowed  to  remain  a  year  as 
a  test  of  success. 

These  may  be  renewed  as  worn  out  if  desirable,  or  a  portion  of 
the  covering  filling  may  be  cut  away  and  metal  introduced.  In  case 
a  plastic  filling  is  desirable  in  any  event,  the  operation  is  to  be  com- 
pleted at  the  time  of  capping  or  at  a  sidxsequent  sitting. 

The  materials  used  with  success  as  pulp  cappers  are: 

1.  A  mixture  of  oil  of  cloves  and  zinc  oxide  (equal  parts  of  car- 
bolic acid  and  oil  of  cloves  may  be  used  as  the  menstruum).  Hub- 
buck's  zinc  oxide  or  cement  powder  may  be  used.  This  is  mixed  to 
a  consistency  which  will  flow,  yet  set  after  some  hours  or  days. 

2.  Oxysulphate  of  zinc,  the  fluid  of  which  is  a  saturated  solution  of 
zinc  sulphate  in  water.  The  powder  is  uncalcined  zinc  oxide.  This 
will  make  a  thin,  creamy  paste  which  flows  readily  and  sets  quickly. 
A  trifle  of  aristol,  iodoform,  or  hydronaphthol  may  be  added. 

3.  Plaster  of  Paris  mixed  with  a  1  per  cent,  solution  of  formaldehyde 
in  water  will  make  an  antiseptic,  quick-setting  paste. 

4.  "Formagen."  This  substance  is  said  to  have  a  mixture  of 
eugenol  and  carbolic  acid  for  the  fluid,  while  the  powder  is  of  zinc 
oxide,  containing  paraform,  the  solid  form  of  formaldehyde.  A  cement 
is  formed  which  sets  quickly  and  must,  therefore,  be  made  very  thin 
when  placed  in  the  cap.  This  material  seems  to  have  l)een  somewhat 
successful  as  a  capper  even  in  exposures  by  caries,  owing  to  its  intense 
germicidal  power.  It  is  claimed  that  the  formaldehyde  penetrates  the 
tissue  of  the  ])ulj)  for  a  distance,  yet  permits  its  return  to  normality. 

Oxychloride  of  zinc,  with  the  fluid  diluted  with  50  per  cent,  of 
distilled  water  (1  to  2),  will  cap  successfully.  It  is  well  to  add  a  little 
powdered  thymol  to  lessen  irritation  and  add  antisepsis. 

Some  positive  claims  are  made  for  crystallized  thymol  as  a  capping. 
It  can  be  gently  melted  on  the  end  of  a  burnisher  and  dropped  on  the 
point  of  exposure  to  crystallize,  or  a  {)iece  of  a  mixture  of  thymol  and 
25 


386  DENTAL  CARIES 

zinc  oxide,  made  by  melting  the  former  and  incorporating  the  latter, 
may  be  added  to  the  drop  of  thymol  in  position  and  melted  with  a 
warm  burnisher.     Setting  cappers  may  be  used  without  metal. 

Results  of  Capping. — If  pain  be  initiated  when  the  cap  is  placed 
and  recur  later,  compression  has  occurred,  and  the  capping  must  be 
removed,  the  pulp  quieted,  and  the  capping  renewed  or  the  pulp 
removed.  Though  no  sensation  be  produced  at  the  time  of  operation, 
a  reaction  to  thermal  changes  may  occur.  If  this  gradually  subside 
as  counterirritants  are  used,  a  diagnosis  of  arterial  hyperemia  (aseptic) 
is  confirmed.  If  the  reaction  increase  and  heat  become  more  irritating 
than  cold,  and  if  at  the  same  time  paroxysms  of  pain  or  reflex  pain 
occur,  the  diagnosis  is  that  of  venous  hyperemia  or  infective  inflam- 
mation, according  to  the  character  of  the  symptoms,  and  the  pulp 
must  be  removed.  In  cases  of  incomplete  roots  the  large  foramen 
prevents  the  formation  of  a  venous  stasis.  Even  if  the  pulp  be  kept 
alive  only  until  root  completion,  much  good  will  be  done.  As  an 
example,  in  one  case  a  lower  second  molar,  exposed  by  caries  and 
capped  at  the  age  of  fourteen,  at  nineteen  years  reacts  as  vital  to 
an  interrupted  electric  current,  and  is  perfectly  comfortable. 

A  pulp  may  remain  quiescent  for  weeks  or  months  and  then  un- 
favorable symptoms  set  in,  or  it  may  die  without  any  apparent  pain. 
It  is  probable  that  in  the  latter  case  some  reflex  pains  have  been  felt, 
but  not  related  with  the  tooth,  in  the  mind  of  the  patient. 

In  the  successful  cases,  either  the  orifice  of  exposure  is  covered  over 
by  a  deposit  of  secondary  dentine,  or  the  pulp  remains  perfectly 
quiescent  beneath  the  capping  material,  without  formation  of  deposit. 

Even  when  a  deposit  occurs  the  pulp  may  die  from  the  atrophy 
and  degeneration  attendant  upon  the  formation  of  much  secondary 
dentine,  and  when  no  deposit  occurs  infection  following  leakages 
about  filling  and  capping  materials  may  take  place  after  years  of 
apparent  success. 

While  capping  may  be,  and  has  been,  successful  in  all  grades  of 
exposure,  there  is  no  certainty  of  success  in  the  exposures  by  caries. 
The  tentative  treatment  necessary  offsets  the  labor  of  canal  treatment. 


THERAPEUTICS  OF  PERFORATION  OF  CARIES. 

The  progress  of  secondary  caries  about  the  pulp  chamber  hollows 
out  the  root  until  at  least  at  one  point  the  chamber  wall  is  but  a  deeal- 


THERAPEUTICS  OF  PERFORATION  OF  CARIES 


387 


cified  layer  of  cementum  covered  by  decomposing  dentine.  At  some 
point  the  pericemental  tissue  will  be  uncovered  by  excavation  or  by  the 
carious  process  (Fig.  315).  The  crown  will  probably  be  hopelessly 
decayed.  Taking,  as  an  example,  a  lower  molar  perforated  at  the 
bifurcation  with  the  pericemental  tissue  hypertrophied  into  the 
opening  (fungous  gum),  its  treatment  may  be  described  as  follows: 
The  gum  is  first  to  be  pressed  out  with  cotton  medicated  with  an 
antiseptic  varnish.  Fletcher's  carl)olize(l  resin,  or  aristol  in  chloro- 
form, or  sandarac  varnish  plus  orthoform  will  serve. 

If  immediate  work  be  desired,  polypoid  fungous  gum  may  be  satu- 
rated with  trichloracetic  acid  and  cut  away  without  bloodletting  by 
means  of  a  large,  sharp  spoon  excavator,  or  cocaine  or  ethyl  chloride 
may  be  used  for  local  anesthesia.  Large,  rose-head  burs  are  used  to 
free  the  cavity  of  all  decay.     The  canals  are  opened  and  treated.     If 


Fig.  329 


Fio.  330 


Diagram  of  treatment  of  perforation 
by  decay. 


Crowning  of  divided  roots. 
(Evans.) 


further  treatment  be  desired,  or  be  impossible  until  the  perforation 
is  disposed  of,  metal  or  wooden  pegs  are  placed  in  the  canals  and  a 
reasonably  thin  layer  of  copper  amalgam  is  built  about  the  pins  and 
over  the  perforation.  A  slight  movement  of  the  pegs  will  permit  their 
withdrawal,  leaving  openings  in  the  amalgam  through  which  the 
treatment  may  be  subsequently  conducted.  The  amalgam  is  then 
allowed  to  harden  (Fig.  329). 

After  canal  filling  the  canals  may  be  further  reamed  for  screws  or 
pins,  which  are  inserted  and  the  operation  completed  with  amalgam 
or  zinc  phosphate  if  the  condition  of  the  crown  admit  of  it ;  or,  if  crown- 
ing be  required,  this  is  arranged  for  in  the  building  up  with  amalgam. 

A  long  perforation  at  a  bifurcation  may  practically  divide  molar 
roots.  This  is  to  be  made  a  complete  division  after  treatment  of  the 
canals.  Each  section  may  be  fitted  with  a  pin  and  amalgam  stump 
to  which  a  gold  barrel  is  fitted.     The  barrels  are  each  given  an  occlusal 


388 


DENTAL  CARIES 


Fig.  331 


face,  or  the   two   a   common  occlusal  face,   and  soldered  together 

(Fig.  330). 
If  one  root  be  unsuitable  it  may  be  extracted  and  the  other  used 

as  a  foundation   for   a  cantilever  crown,  a  spur  from  which  rests 

slightly  upon  the  occlusal  face  of  the  adjoining  tooth  (Fig.  331). 
A  smooth  plaque  of  low-heat,  white  gutta-percha  (not  temporary 

stopping)  makes  an  excellent  covering  for  a  perforation.     It  is  made 

larger  than  the  opening  to  be  cov- 
ered, pressed  to  place,  and  the  edges 
sealed  with  a  hot  burnisher.  The 
covering  filling  will  retain  it  in  posi- 
tion. The;  approach  to  the  per- 
foration should  be  widely  funnelled 
to  permit  a  ready  adaptation.  If 
sepsis  occur,  the  resulting  abscess 
will  occur  opposite  the  perforation, 
or   in    some    cases  create  a    small 

pocket  similar  to  a  pyorrhea  pocket.     In  all  cases  judgment  must 

be  exercised  and  the  attempt  to  conserve  unsuitable  cases  avoided. 


Cantilever  crown.     (Evans.') 


THERAPEUTICS  OF  LOSS  OF  CROWN  BY  CARIES. 

If  the  portion  of  crown  left  after  excavation  be  self-sustaining,  but 
incapable  of  retaining  a  filling,  pins  or  screws  may  be  placed  in  the 
root  canal  or  the  pulp  cavity  may  be  enlarged  and  made  retentive. 
A  filling  is  then  built  about  or  into  the  anchorage  so  made.  At  times 
the  remainder  of  a  tooth  crown  will  support  a  hollow  metal  crown. 

When  the  carious  crown  has  broken  away  or  filling  has  become 
practically  impossible  or  undesirable,  the  original  beauty  or  useful 
form  of  the  tooth  may  be  approximately  restored  by  means  of  one  of 
the  many  forms  of  dowelled  porcelain  crowns,  specially  constructed 
gold  and  porcelain  crowns,  or  all-gold,  hollow-metal  crowns,  or  a 
broad  band  may  be  adjusted  and  filled  in  with  amalgam  after  setting 
with  cement. 

If  an  anterior  root  be  so  hollowed  out  by  caries  as  to  be  incapable 
of  supporting  a  dowelled  crown,  it  may  be  extracted  and  the  operation 
of  transplantation  performed,  or,  later,  an  implantation  may  be  made. 

In  the  former  operation  the  existing  alveolus  is  enlarged  if  neces- 
sary to  accommodate  a  tooth;  in  the  latter  operation  a  new  alveolus  is 


'  Artificial  Crown  and  Bridge  Work. 


THERAPEUTICS  OF  LOSS  OF  ROOT  BY  CARIES  389 

created  by  means  of  appropriate  trephines  and  reamers.  The  tooth 
is  to  be  prepared  as  for  rephmtation  (which  see).' 

If  teeth  have  been  lost  by  extraction,  the  spaces  created  may  be 
filled  by  means  of  bridge-work  or  plates  of  various  sorts. 

By  common  consent  crown  and  bridge  work  is  considered  a  special 
department  of  dentistry. 

Therapeutics  of  Loss  of  Root  by  Caries. — This  occurs  in  several  ways: 

1.  After  loss  of  the  crown  and  the  extension  of  the  carious  process 
into  the  interior  of  the  root.  In  the  later  stages  this  root  is  rendered 
valueless  for  crowning  purposes,  and  should  be  extracted.  In  some 
cases  a  transplantation  operation  would  be  warrantable,  as  in  case 
of  a  single  incisor,  the  other  teeth  being  relatively  sound. 

2.  If  an  artificial  crown  has  been  so  placed  as  to  expose  the  joint 
to  caries,  the  process  may  proceed  to  a  considerable  extent,  but  does 
not  necessarily  involve  the  root  interior  owing  to  the  presence  of  the 
pin.  Filling  with  amalgam  or  other  plastic,  or  the  recrowning  is 
demanded  if  feasible.  The  gum  having  grown  in,  much  packing 
out  may  be  required;  lancing  may  be  required  as  well. 

3.  In  some  cases  penetrating  cervical  caries  will  cause  a  partial  or 
complete  amputation  of  a  palatal  or  buccal  root  of  an  upper  molar, 
or,  possibly,  a  bicuspid.  The  pulp,  of  course,  will  have  died,  at 
least  at  the  carious  area. 

The  cavity  of  decay  should  be  cleansied  and  undercut,  and  an 
occlusal  tap  made  for  free  entrance  to  the  canals.  The  canals  are  to 
be  reamed  with  Downie  broaches.  The  canal  of  the  decayed  root 
is  to  be  enlarged  with  Gates-Glidden  drills,  after  which  everything  is 
to  be  dried;  a  canal  probe  is  passed  through  the  tap  across  the  cavity 
into  the  farther  portion  of  the  root  canal.  Good  amalgam  is  to  be 
thoroughly  packed  into  the  cervical  cavity  and  hardened  by  wafering. 
When  nearly  set,  the  canal  probe  is  carefully  withdrawn.  After 
appropriate  sterilization  of  canals  with  formalin  solutions,  and  the 
filling  of  canal  apices,  an  iridioplatinum  pin  is  to  be  cemented  into 
the  involved  canal  and  crown  tap,  thus  strengthening  the  root  against 
a  threatened  fracture. 

If  actually  separated  by  decay,  excavation  will  make  an  open  joint, 
which  should  be  filled  with  amalgam  after  the  pin  has  been  run 
through  the  tap  into  the  root.  If  this  operation  does  not  seem 
feasible,  it  is  better  to  extract  the  separate  root  ])ortion  and  trim  the 
stump,  as  in  ordinary  root  amputation. 

1  For  methotl.s  of  implantation,  see  American  Text-book  of  Oppnitivp  Dentistry. 


390  DENTAL  CARIES 

While  the  retention  of  an  amputated  root  is  seldom  demanded,  the 
editor  has  several  in  satisfactory  use.  The  prevention  of  a  threatened 
fracture  is  more  often  demanded.     (See  also  Heteroplasty.) 


CARIES  OF  THE  TEMPORARY  TEETH. 

Caries  of  the  temporary  teeth  differs  but  little  from  that  of  the 
permanent  teeth.  The  pulp  cavities  are,  however,  relatively  larger, 
and  the  intensity  of  the  carious  process  often  causes  rapid  exposure 
of  the  pulp.  Owing  to  the  flat  character  of  the  approximations  of 
the  teeth,  there  is  often  more  approximal  than  occlusal  caries,  and 
the  cavities  often  have  weak  peripheries. 

Children  have  a  fear  of  dental  offices,  excited  by  unpleasant  experi- 
ences or  the  talk  of  their  elders,  and  they  do  not  mention  slight  pain 
such  as  that  excited  by  hypersensitive  dentine.  There  is,  however, 
abundant  evidence  that  the  dentine  of  the  temporary  teeth  may  be 
hypersensitive.  In  cavities  of  simple  nature  the  fillings  indicated 
for  adults  serve  if  the  operations  are  well  borne. 

The  shapes  of  the  teeth,  the  restlessness  and  fear  of  the  little  patients, 
and  the  free  flow  of  saliva  indicate,  for  the  most  part,  the  use  of  plastic 
fillings,  though  the  rubber  dam  may  often  be  readily  used.  In  deep 
cavities  not  exposing  the  pulps  the  methods  employed  for  adults,  of 
varnishing  or  insulating  with  gutta-percha  and  the  subsequent  use 
of  zinc  phosphate  as  a  lining  under  metal  fillings,  are  indicated. 
Certain  occlusal  cavities  having  small  orifices  and  large  interiors  are 
well,  and  often  permanently,  filled  with  pink  gutta-percha. 

If  cavities  are  observed  before  pain  has  been  complained  of,  and 
prompt  and  quickly  subsiding  response  to  applications -of  cold  water 
is  obtained,  indicating  a  normal  pulp,  the  cavity  should  be  excavated, 
with  more  regard  to  removing  the  marginal  caries  than  to  thorough 
excavation,  dried,  and  an  application  of  a  20  per  cent,  solution  of 
silver  nitrate  made  for  a  few  minutes,  the  cavity  being  subsequently 
filled. 

In  cases  of  adjoining  approximal  cavities  there  is  a  disposition  for 
the  affected  teeth  to  press  together  and  lessen  the  size  of  the  dental 
arch.  Bonwill  advised  as  a  practice,  followed  by  uniformly  good 
results  in  such  cases,  to  cleanse  the  cavities  (Fig.  332)  and  insert 
masses  of  pink  gutta-percha  base-plate.  The  constant  biting  upon 
the  gutta-percha  causes  a  separation  of  the  teeth,  which  increases  the 


CARIES  OF  THE  TEMPORARY  TEETH  391 

size  of  the  arch  and  affords  additional  space  for  permanent  successors. 
Holliiigsworth  introduced  the  idea  of  phioiiif;  a  small  piece  or  cap  of 
metal  at  the  cervix,  bridging  the  interdental  space.  A  bit  of  gutta- 
percha is  to  be  placed  on  the  under  side  of  the  caps  to  make  a  gutta- 
percha adaptation;  then  more  is  built  over  it.  Bonwill  advised  that 
before  the  gutta-percha  masses  are  inserted  small  pieces  of  blotting 
paper  saturated  with  carbolic  acid  be  laid  against  tiie  dentinal  walls 
and  the  gutta-percha  be  packed  over  them.  The  more  efficient  and 
persistent  antiseptic  silver  nitrate  may  be  applied  instead  of  the  car- 
bolic acid.  Kirk  advises  that  asbestos  felt  be  heated  to  destroy  any 
organic  matter  present  in  it  which  might  combine  with  the  silver, 
and  then  be  soaked  in  a  saturated  solution  of  silver  nitrate,  dried, 
and  kept  in  dark  bottles  away  from  the  light.  Small  pieces  of  the 
prepared  felt  may  be  used  as  descril)ed.  With  cavities  as  good 
as  shown  in  the  illustration,  wedging  and  contour- 
ing each  tooth  with  amalgam,  after  the  use  of  silver  ^'"'  ^^" 
nitrate  and  varnish,  is  quite  admissible  after  making 
suitable  retention.  The  conditions  will  determine 
the  choice  of  materials. 

The  silver-nitrate  method  is  particularly  appli- 
cable to  shallow  cavities  in  which  excavation  for 
filling  is  impracticable.      The  dentine  surface   is     ^'"'^^  "/  p^i'^ring  ap- 

"  '  proximal  cavities. 

cleansed  and  dried,  and  the  fused  silver  nitrate  is 
rubbed  upon  the  surface.  This  may  be  done  after  the  method  of 
Craven:  a  platinum  wire  is  dipped  into  the  powdered  salt  and  held 
over  a  flame  until  the  ])owder  fuses  into  a  button.  By  this  means 
application  can  be  directly  and  accurately  made.  The  arch  is  apt  to 
become  somewhat  contracted,  and  food  is  liable  to  wedge  between 
the  teeth.  Combination  fillings  of  zinc  phosphate  or  oxyphosphate 
of  cop])er  and  amalgam  are  of  advantage  in  case  of  frail  walls. 

For  the  anterior  teeth  zinc  phosphate  and  gutta-])ercha  fillings  are 
useful,  and  for  the  posterior  ones  Ames'  oxyphosphate  of  copper 
serves  a  good  purj)()se. 

Cari(\s  is  very  liable  to  occur  upon  the  approximal  surfaces  of  the 
second  temj)orary  antl  first  ])ermanent  molar.  If  the  former  be  found 
largely  decayed  distally,  the  latter  will  usually  be  found  decayed  on 
the  mesial  surface.  Amalgam  in  cavities  well  extended  buccally 
and  lingually,  or  gutta-percha,  serves  well  until  the  second  temporary 
molar  is  lost,  when  a  good  gold  filling  may  often  be  introduced 
before  the  second  bicuspid  erupts. 


392  DENTAL  CARIES 

Well-contoured  fillings  must  be  inserted  in  such  a  case.  As  a  pre- 
ventive measure  during  eruption  of  the  first  molar,  the  second  tem- 
porary molar  may  be  disked  to  the  form  shown  in  Fig.  333. 

If  incipient  or  simple  decay  have  occurred  on  the  two  teeth,  or  even 
the  second  molar  alone,  it  is  then  best  to  wedge  the  teeth  apart  and  to 
make  a  disk  separation  (on  the  temporary  tooth  only)  from  the  lingual 
or  buccal  side,  or  both,  and  to  contour  the  filling  even  in  exaggera- 
tion, so  that  a  minimum  of  contact  shall  exist.  Any  surface  of 
dentine  exposed  by  the  disking  should  be  included  in  the  cavity,  or, 
if  this  be  not  possible,  then  it  should  be  rubbed  with  silver  nitrate. 

Fig.  333 


Right  upper  temporary  molar  disked  liiigually  and  filled. 

Such  surfaces  sliould  be  carefully  observed  at  regular  intervals; 
indeed,  if  prophylactic  treatment  can  be  regularly  instituted  early  and 
before  caries  of  the  first  permanent  molar,  much  good  will  be  done. 

The  J)iill)  diseases  resulting  from  caries  of  the  temporary  teeth  will 
be  considered  with  those  of  the  permanent  teeth.  If  the  temporary 
teeth  be  so  badly  decayed  as  to  be  hopeless,  so  far  as  filling  is  con- 
cerned, they  should  be  extracted.  Occasionally  the  encircling  of  the 
teeth  with  pure  gold  bands  cemented  to  place  or  filled  in  with  amal- 
gam is  good  practice. 

In  the  main  the  temporary  teeth,  especially  the  molars,  should  be 
filled  with  some  view  to  the  longevity  of  the  fillings,  as  they  often  have 
to  do  service  for  years,  and  the  general  health  of  the  mouth  is  improved. 


RECURRENCE  OF  CARIES  393 

The  child  should  always  be  treated  with  kindness  and  truthfulness 
to  establish  faith,  yet  with  sufficient  firmness  to  command  coijtrol. 

Under  no  circumstances  should  the  child  be  given  an  excessive 
dread  of  dental  operations,  or  i^e  broken  by  nervous  shock,  as  this 
attitude  defeats  the  object  sought. 

RECURRENCE  OF  CARIES. 

Passing  over,  as  disproved  by  Miller,  the  theory  of  Palmer,  that  caries 
recurs  about  fillings  as  the  result  of  electric  action,  it  may  be  stated, 
as  proved  by  scientific  and  clinical  experience,  that  it  recurs  because 
after  teeth  have  been  filled  conditions  exist  which  may  favor  the 
collection  of  microbic  plaques  and  stagnant  food  material  even  more 
strongly  than  the  original  conditions,  and  that  when  recurrence  has 
been  prevented  the  work  has  been  done  in  such  a  manner  as  to  pre- 
vent such  collections. 

The  specific  defects  which  favor  the  formation  of  bacterial  placjues 
may  be  epitomized  as  follows : 

1.  Lack  of  approximal  contact  (food  wedging  between  teeth). 

2.  Roughness  of  the  filling  at  an  otherwise  good  approximal  contact 
point  which  menaces  the  approximating  tooth  or  the  margin  of  the 
cavity  by  causing  food  retention  and  the  spreading  of  microbic 
plaques. 

3.  Unremoved  excess  of  filling  material  at  margins  producing  a 
ledge  which  collects  food,  etc.  The  edge  of  a  crown  may  act  in  a 
similar  manner.  An  excess  well  beneath  the  gum  is  more  apt  to 
produce  gingivitis  than  caries. 

4.  Exposure  of  the  cavity  margin  due  to  lack  of  covering  by  the 
filling  material,  whether  not  properly  placed,  flaked  away,  or  due  to 
fracture  of  margin  during  the  filling  process  or  subsequently  thereto. 

5.  Exposure  of  the  cavity  margin  due  to  shrinkage  or  shifting  of 
the  filling  material.  The  use  of  material  not  enduring  mastication 
in  places  subject  to  it;  the  washing  out  of  cement  from  the  joint  of 
an  inlay  or  combination  filling  or  dowelled  bandless  crown  has 
much  the  same  efi'ect,  though  often  much  delayed. 

G.  Solubility  of  the  filling  material,  permitting  the  cavity  wall  to 
become  exposed. 

7.  Roughness  of  tooth  surface,  produced  by  polishing  fillings  with 
rough  approximal  trimmers,  coarse  grit  strips,  disks,  or  wIh'cIs. 
Exposure  of  dentine  by  overpolishing  may  be  classetl  with  the  above. 


394  DENTAL  CARIES 

8.  Lack  of  hygiene  of  surfaces  which  tend  to  decay,  partly  due 
to  lack  of  extension  of  cavity  margins.  Even  poor  margins,  if  well 
extended,  may  not  decay,  whereas  existing  at  or  near  contacts  they 
are  menaces.  Lack  of  extension  of  a  filling  into  a  fissure  adjoining 
it,  which  fissure  may  be  decayed  or  invite  subsequent  decay. 

Treatment. — The  treatment  of  recurrent  caries  does  not  differ 
materially  from  that  of  primary  caries. 

Repairs  to  obliterate  crevices,  breaks,  or  new  decays  may  at  times 
be  made,  but  so  often  is  it  the  case  that  apparently  slight  recurrences 
are  found  after  removal  of  the  filling  to  involve  the  entire  cavity  wall, 
that  the  only  sound  recommendation  applicable  to  all  cases  is  that 
the  filling  be  removed  and  the  cavity  reprepared  and  refilled.  The 
exception  exists  when,  after  the  new  cavity  of  decay  is  all  excavated, 
the  adaptation  of  the  filling  is  seen  to  be  perfect.  Decay  at  two  or 
more  points  of  recurrence  or  general  inferiority  of  the  filling  should 
condemn  the  entire  piece  of  work. 


PROPHYLAXIS  OF  CARIES. 

If  the  factors  of  caries  be  removed  from  the  mouth,  caries  cannot 
occur.  That  a  clean  tooth  will  not  decay  is  a  dictum  many  years 
established.  The  microbic  plaques  and  fermentable  food  substances 
acting  as  the  causes  of  caries  should,  therefore,  be  kept  from  collecting 
upon  the  teeth. 

In  the  absence  of  absolutely  exact  knowledge  of  the  relation  of 
general  systemic  conditions  to  the  production  of  microbic  plaques,  it 
may  be  said  that  the  general  health  should,  if  possible,  be  maintained 
by  the  correction  of  any  morbid  body  state,  as,  without  doubt,  perfect 
good  health  is  a  corrective  of  morbid  oral  secretions.     (See  p.  318,  etc.) 

Apart  from  this,  oral  cleanliness  is  of  great  importance,  not  only 
for  the  health  of  the  teeth,  but  of  the  gums,  and,  indirectly,  of  the 
stomach  and  intestines,  which  can  but  be  affected  by  unhealthy  oral 
conditions.  Thus,  while  the  general  health  may  influence  the  mouth, 
the  mouth  may  influence  the  general  health. 

It  has  l)een  noted  that  caries  is  markedly  lessened  in  well-kept 
dentures. 

The  first  stej)  in  the  prevention  of  caries  is  the  removal  of  all  possible 
causes  of  bacterial  plaque  formation.  Cavities  should  be  obliterated 
by  means  of  exactly  adapted,  perfectly  contoured,  highly  polished. 


DAILY  CLEANSING  OF  THE  TEETH  395 

insoluble  (in  so  far  as  utilizable)  filliiii^s,  the  margins  of  whicli  are 
extended  into  areas  subjected  to  friction  by  ordinary  means.  De- 
partures from  this  principle  are  to  be  made  for  well-judged  reasons 
only. 

Black  kept  a  record  of  caries  of  the  enamel  over-riding  the  angle 
from  the  approximal  surface  to  the  buccal  or  lingual,  and  found  that 
it  occurred  only  in  about  one  case  in  a  thousand  persons.  He  had 
previously  concluded  that  these  angles  were  areas  of  relative  immunity 
kept  so  by  food  and  brush  excursions,  and  that  if  ])ossible  the  cavity 
should  be  extended  to  and  not  beyond  the  angle. 

Hoffheinz  claims  that  it  is  not  so  much  a  fjuestion  of  extension, 
but  of  contouring  to  prevent  the  contact  of  margins. 

By  these  means  centres  of  infection  are  removed,  and  tiie  problem 
is  reduced  to  the  care  of  the  superficies  of  the  teeth.  Calculus  should 
be  thoroughly  removed,  the  teeth  highly  polished  and  kejjt  polished. 
This  operation  mechanically  removes  the  plaques. 

To  prevent  their  return,  daily  cleansing  of  the  teeth  by  tlie  patient 
has  always  been  practised,  and  a  thorough  cleansing  once  a  month 
or  oftener  by  the  operator  has  been  shown  by  I).  1).  Smith  to  be 
highly  efficacious. 


DAILY  CLEANSING  OF  THE  TEETH. 

A  well-made,  stiff  brush,  having  a  lengthened  tuft  of  bristles 
at  its  tip  and  its  brushing  surface  serrated,  is  to  be  moistened  and 
well  charged  with  a  good  antiseptic  tooth-powder  or  paste.  Tt  is  to 
be  grasped  in  the  palm  of  the  hand  with  the  ball  of  the  thumb  placed 
upon  the  back  of  the  handle,  or  exactly  the  reverse,  acconhng  to  the 
movement  desired.  The  bristles  are  to  be  passed  over  the  buccal  and 
lingual  surfaces  of  the  teeth,  from  the  gum  toward  the  occlusal  sur- 
faces, by  means  of  a  dexterous,  wiping  motion  imparted  by  a  turn  of 
the  wrist.  This  cleanses  the  interproximal  spaces  so  far  as  accessible 
to  the  brush.  By  a  light  to-and-fro  motion  the  lingual  and  buccal 
crevices  are  freed  of  soft  deposits  which  occur  after  each  meal.  Uidess 
the  gums  be  actually  torn,  this  light  friction  is  not  injurious.  Hspiuial 
attention  is  to  be  paid  to  the  buccal  surfaces  of  third  molars,  which 
are  often  ignored  even  by  conscientious  patients. 

The  lingual  surfaces  of  incisors  are  cleansed  by  means  of  the  still" 
tip  of  the  brush.     In  cases  of  advanced  recession  of  tlit>  gum  al)out 


396  DENTAL  CARIES 

incisors,  a  brush  with  all  the  bristles  except  those  of  the  tip  cut  away 
is  advantageous.  This  is  also  useful  for  the  lingual  surfaces  of  bridge- 
work.     Occlusal  surfaces  are  to  be  freely  brushed. 

A  light  brushing  after  each  meal  imparts  to  the  mouth  a  pleasing 
sense  of  cleanliness,  which  has  a  good  moral  effect  upon  the  patient, 
and  removes  from  about  the  teeth  much  fermentable  material. 

The  teeth  should  be  thoroughly  brushed  upon  retiring  with  a  tooth- 
powder  containing  castile  soap  and  free  from  coarse  grit,  as  pumice  or 
coarse  chalk,  to  remove  any  debris  about  the  teeth,  and  the  antiseptic 
and  antacid  treatment  to  be  mentioned  employed.  Salol  should  be 
omitted,  because  of  its  tendency  to  produce  labial  eczema;  while 
aromatically  agreeable,  it  has  little  antiseptic  value.  A  small  rubber 
band  should  be  stretched  between  the  teeth,  the  inner  end  released, 
and  then  drawn  through  the  interdental  space,  wiping  the  approximal 
surfaces  and  embrasures.  This  places  the  mouth  in  a  fairly  aseptic 
state  for  the  night,  during  which  the  oral  fluids  are  at  rest  and  less 
interfere  with  fermentation  or  neutralize  its  products. 

Before  breakfast  the  mouth  should  again  be  treated  with  the  brush 
and  antiseptic  to  remove  the  bacteria  developed  during  the  night. 

Once  a  week  the  patient  should  dip  floss  silk  in  the  tooth-powder 
(or  rub  the  powder  over  the  interproximal  spaces),  carry  it  between 
the  teeth  and  rub  the  approximal  surfaces,  with  the  object  of  removing 
any  bacterial  collection  upon  these  surfaces. 

The  floss  silk  should  not  be  forced  into  the  gum,  as  this  will  injure 
the  gum  margins  and  force  infected  material  into  it,  but  should  be 
first  carried  gently  beneath  the  gum,  wrapped  half  around  the  tooth, 
and  then  sawed  up  over  the  contacts  and  be  brought  out  from 
between  the  teeth. 

After  cleansing  the  teeth  at  night  an  antiseptic  should  be  held  in  the 
mouth  for  the  space  of  two  minutes,  for  the  purpose  of  devitalizing 
bacteria  present.  For  this  purpose  phenol  sodique  in  12.5  per  cent, 
solution  in  water  (1  to  7)  is  as  valuable  as  any  agent,  though  many 
harmless  and  effective  preparations  are  sold  for  this  purpose. 

In  a  mouth  especially  prone  to  caries  of  the  teeth  it  is  well  to  use, 
once  or  twice  a  week,  a  disguised  mercuric  chloride  wash,  1  to  2000, 
for  the  space  of  two  minutes.  The  object  is  to  thoroughly  devitalize 
oral  organisms  and  promote  the  action  of  the  milder  and  more  agree- 
able antisej)tics. 

The  following  is  a  useful  formula:^ 

*  C,  R.  Jackson,  Dental  Summary,  1904. 


DAILY  CLEANSING  OF  THE  TEETH  397 

I^. — Mercuric  chloride gr.  vi 

Tliymol gr.  ij 

Menthol gr.  v 

Oil  eucalyptus gtt.  x 

Glycerin fS'J 

Alcohol fSiJ 

Aqua;  Gaultheris ad  oij— M. 

S. — Use  as  directed  as  mouth  wash. 

Finally,  after  the  above  treatment,  Phillips'  milk  of  magnesia 
(magnesium  hydrate  in  suspension)  should  he  taken  in  eoneentrated 
form  into  the  mouth,  rinsed  about  and  drawn  by  suetion  between  the 
teeth.  The  excess  is  to  be  expectorated  and  the  residue  left  in  the 
mouth.  It  is  alkaline,  slightly  astringent,  and  is  credited  with  some 
antiseptic  property.  These  processes  do  not  consume  much  time  if 
the  patient  l)e  systematic.  The  brush  itself  should  be  sterilized  after 
using.  A  0.3  per  cent,  solution  of  formaldehyde  may  be  placed  in  a 
test-tube  conveniently  hung,  and  be  renewed  freely.  In  this  the  brush 
may  remain  until  again  needed,  or  it  may  be  later  removed  and  dried. 

Dr.  Percy  R.  Howe  calls  attention  to  the  valuable  attributes  of  a 
1  per  cent,  solution  of  sodium  sulphate,  followed  by  a  1  per  cent, 
solution  of  sodium  bicarbonate,  in  the  dissipation  of  coagula  and 
mucinous  collections  in  the  mouth,  rendering  the  saliva  clear  and 
limpid.^  Lime  water  also  removes  this  viscidity,  so  that  the  virtue 
seems  to  reside  in  the  antacid  or  alkaline  quality  of  the  substance. 

The  periodical  cleansing  suggested  by  1).  D.  Smith  involves  the 
monthly  rubl)ing  down  of  all  surfaces  accessible  to  a  wedge-shaped 
wooden  polishing  point  directed  by  a  hand  carrier.  Powdered  pumice 
is  the  abrasive  suggested.  The  point  is  to  be  gently  insinuated 
beneath  the  free  gum  margin  for  the  purpose  of  effecthig  a  cleanliness 
there,  which  shall  prevent  collections  liable  to  produce  pyorrhea 
alvcolaris. 

This  method  may  be  supplemented  by  a  careful  riil)l)ing  down  of 
contact  points  by  means  of  floss  silk  charged  with  powdered  pumice 
as  an  additional  precaution  against  approximal  caries. 

The  slight  cleansing  apparently  required  after  a  few  visits  is  a 
strong  argument  in  favor  of  these  prophylactic  cleansings.  In  case  of 
fairly  cleanly  mouths  free  of  other  disease  than  caries  the  patient  may 
be  instructed  in  the  use  of  a  wood  point  held  in  a  simple  porte- 
polisher,  such  as  a  tube  of  thin  nickelled  brass  bent  at  one  end  to 
an  angle  of  45  degrees,  and  the  prophylaxis  by  the  operator  executed 
three  or  four  times  a  year  only. 

'  Dental  Cosmos,  1905. 


398  DENTAL  CARIES 

Periodical  examinations  should  be  made  at  short  intervals,  pref- 
erably at  the  time  of  cleansing,  for  cavities  of  decay,  roughness  of 
filling  margins,  or  accidents  to  the  same.  By  these  means  the  soil 
may  be  rendered  unsuitable  to  the  growth  of  caries  fungi,  and  their 
localization  at  the  contacts  and  other  favoring  spots  is  largely  pre- 
vented. 

Silver  nitrate,  40  per  cent,  to  saturated  solution,  may  be  applied  to 
surfaces  likely  to  decay,  as  sulci,  contact  points,  etc.,  as  a  means  of 
prevention  in  mouths  subject  to  same.^ 

Some  dentists  pursue  the  policy  of  filling  only  the  larger  cavities 
existing  in  a  mouth,  the  others  being  neglected  until  a  subsequent 
period.  Such  a  method  is  to  be  condemned  as  being  a  neglect  of  a 
plain  duty  and  as  tending  to  the  propagation  of  caries  in  the  mouth. 
The  presence  of  cavities,  calculus,  and  pyorrhea  alveolaris  in  the 
mouth  all  tend  to  cause  infection  of  the  digestive  tract,  with  produc- 
tion of  inflammatory  (catarrhal)  disturbance,  and  to  cause  infection 
of  parts  in  close  association  with  the  teeth  as  well. 

Undoubted  cases  of  septic  intoxication  and  infection  from  decayed 
teeth  and  other  oral  conditions  have  been  reported,  the  connection 
having  been  shown  by  their  cure  after  removal  of  the  local  cause 
alone;  in  other  cases  the  parts  (as  the  stomach)  having  the  second- 
ary infection  well  implanted,  have  required  special  antisepic  treat- 
ment in  addition  to  the  removal  of  the  primary  exciting  cause.  ^  (See 
Systemic  Effects  of  Pyorrhea  Alveolaris.) 

The  evils  attendant  upon  sepsis  are  to  be  pointed  out  to  patients 
who  have  often  a  seeming  indifi^erence  to  conditions  ranging  from 
simple  uncleanliness  to  loathsome  filth  within  the  mouth,  which 
would  alarm  them  if  existing  in  any  other  part  of  the  body.  Aside 
from  all  considerations  of  health  or  tooth  integrity,  it  is  poor  economy, 
and  especially  for  poor  people,  to  neglect  these  measures  which  are 
largely  applicable. 


PROPHYLAXIS  IN  SYSTEMIC  DISEASE. 

During  a  prolonged  illness,  seasickness,  pregnancy,  etc.,  the  pro- 
phylactic care  of  the  teeth  should  bo  rigidly  enforced  as  a  means  of 
preventing  decay  of  the  teeth  and  sepsis  of  the  mouth. 

'  L.  C.  Bryan  and  other.s. 

2  Hunter,  International  Dental  Journal,  1899.  Abwtract  from  Transactions  of  Odontological 
Society  of  Great  Britain. 


PROPHYLAXIS  IN  SYSTEMIC  DISEASE  399 

It  has  been  shown  that  ckiring  pregnancy  osteomalacia  may  occur, 
and  that  it  represents  a  deininerahzation  by  decalcification  of  the  hones 
of  the  mother.  Whether  or  not  this  may  influence  caries  of  enamel  is 
not  certain,  though  acid  secretions  occur  from  the  gum  margins,  but 
there  is  no  n^ason  why  the  resistance  of  the  fibrils  of  the  dentine  should 
not  be  lessened,  or  even  that  the  dentine  may  not  l)e  to  an  extent 
demineralized,  as  positively  claimed  l)y  some  accurate  observers 
(Black  to  the  contrary).  An  excessive  osteomalacia  may  be  held  to 
represent  a  deficiency  of  osteogenetic  nutritive  material  for  the  child. 
This  would  lead  to  an  inferior  development  of  the  child's  temporary 
teeth. 

Any  abnormal  condition  of  the  mother  should  be  corrected,  if 
possible,  in  order  that  her  general  nutrition  and  that  of  the  child 
may  not  suffer. 

Probably  upon  the  congenital  constitution  of  the  child  depends 
much  of  its  future  susceptibility  or  immunity  to  caries. 

Accepting  the  decalcification  theory  of  osteomalacia,  the  use  of  mild 
alkalies  internally,  such  as  a  tablespoonful  of  lime  water  and  the  u.se  of 
lime-containing  foods,  as  the  cereals,  cannot  but  be  of  value  as  antacids 
furnishing  a  neutralizing  agent  for  the  acid,  while  the  lime  probal)ly 
enters  into  the  development  of  bone  (Hare),  and,  therefore,  would  be 
useful  in  supplying,  via  the  placenta,  mother's  milk  and  food,  the 
element  needed  for  the  development  of  teeth. 

The  teeth  should  receive  all  needful  care  during  pregnancy,  that  the 
mother  should  not  sufl^er  pain,  but  work  should  be  of  a  temporary 
nature,  if  necessary,  to  avoid  shock,  especially  at  about  the  third 
month  of  gestation.  Attention  has  been  called  to  the  fact  that  dur- 
ing menstruation  a  systemic  hyperacidity  exists,  which  can  be  com- 
bated by  the  use  of  lime  internally  and  milk  of  magnesia  locally. 


SECTION   TV. 

DISEASES  OF  THE  DENTAL  PULP. 


CHAPTER  XV. 
CONSTRUCTIVE  DISEASES. 

Diseases  of  tlic  dental  pulp  are  l)oth  acute  and  chronic.  Accord- 
ing to  the  anatomical  features,  they  may  also  be  divided  into  con- 
structive and  destructive.  The  acute  diseases  are  usually  destruc- 
tive; in  the  chronic,  structural  and  constructive  changes  are  connnonly 
noted.  Constructive  diseases  of  the  dental  pulp  are  those  attended  by 
the  formation  of  deposits  of  new  masses  of  calcific  substance.  De- 
structive diseases  are  those  which  cause  retrogressive  and  necrotic 
changes  in  the  tissues  of  the  pulp.  The  essential  difference  between 
the  two  classes  of  diseases  is  in  the  mode  and  character  of  the 
degeneration — the  one  is  acute,  the  other  chronic. 

Pathologically  there  is  no  abrupt  line  of  demarcation  between 
diseases  of  the  dentine  and  those  of  the  pulp,  as  the  dentinal  tubules 
contain  the  fibrillar  prolongations  of  the  odontoblasts  of  the  i)ulp. 
Effects  produced  upon  the  fibrils  cause,  therefore,  a  pulp  reaction 
which  may  lead  either  to  a  construction  or  destructive  activity  accord- 
ing to  the  grade  of  hyperemia  or  inflammation  set  up. 

As  infection  may  travel  via  the  tubules  even  septic  inHannnation 
may  result  before  the  pulp  is  exposed. 

INIoreover,  after  constructive  changes  which  are  accompanied  by 
more  or  less  atrophy  and  degeneration,  the  pulp  may  untlergo  the  more 
acute  destructive  changes.  While  the  exact  relations  between  symptoms 
and  pathology  are  not  all  worked  out  and  the  symptoms  are  often 
obscure,  due  to  the  fact  that  the  pulj)  is  without  the  sense  of  touch  or 
exact  location,  and,  therefore,  the  pains  induced  are  reflected,  as  a  rule, 
yet  clinical  observation  and  the  .r-rays  have  done  much  to  relate  the 
symptoms  and  pathology,  and  one  must  depentl  u{)oii  these  and 
20 


402  DISEASES  OF  THE  DENTAL  PULP 

applied  tests  for  at  least  a  tentative  diagnosis,  of  Avhich  confirmation 
may  be  sought. 

The  pathological  conditions  of  the  pulp  are  judged  by  the  phenom- 
ena induced  by  applications  of  air  or  water  of  varying  temperatures, 
and  by  the  presence  of  certain  appearances  of  the  tooth,  which,  taken 
with  the  symptoms  and  tests,  lead  to  a  fair  inference  of  the  disease 
present. 

It  was  pointed  out  by  Black^  that  if  a  healthy  tooth  be  isolated  by 
a  double  layer  of  rubber  dam,  and  a  jet  of  water  at  a  temperature  of 
40°  F.  be  directed  against  the  tooth,  a  paroxysm  of  pain  is  produced. 
A  jet  of  hot  water  will  also  induce  a  similar  pain,  and  if  the  patient's 
eyes  be  shielded  no  difference  in  the  sensations  is  noted;  that  is, 
the  pulp  responds  to  thermal  stimuli,  hot  or  cold,  indifferently.  The 
organ  is  accustomed  to  variations  of  temperature  between  60°  and 
105°  to  110°  F.,  and  within  this  range,  in  a  condition  of  health,  takes 
no  apparent  cognizance  of  this  degree  of  change. 

With  a  decrease  in  the  amount  of  dentine  covering  the  pulp — e.  g., 
with  the  advance  of  caries — the  reaction  to  thermal  stimuli  increases 
in  promptness,  until,  when  the  pulp  is  nearly  exposed,  the  response  is 
immediate.  Succeeding  this  is  noted  prompt  response  to  lesser  degrees 
of  temperature  change,  until  the  pulp  comes  to  respond  immediately 
to  water  at  a  temperature  of  85°  F.,  or  thereabout,  and  slightly  over 
the  bodily  temperature,  102°  F.  Later,  another  feature  makes  its 
appearance;  instead  of  a  sharp  contraction  pain,  applications  of 
moderate  thermal  stimuli  are  followed  by  a  heavy,  throbbing  pain. 
Later,  similar  pains  occur  in  the  absence  of  tangible  external  sources 
of  irritation.  In  the  ordinary  sequence  of  events  intense  pain  is 
later  caused  by  hot  applications,  and  cold  applications  afford  relief. 

The  response  to  thermal  stimuli  may  pursue  the  opposite  course. 
The  normally  prompt  response  is  followed  by  delays  in  reaction,  until 
it  is  only  after  the  continued  application  of  cold  to  the  exterior  of  a 
tooth  that  a  paroxysm  of  pain  is  induced.  In  these  cases  there  follows 
after  a  long  time  an  increasing  response  to  heat,  as  in  the  former 
instance,  the  reaction  occurring  only  upon  decided  or  prolonged  heat 
stimuli.  Following  upon  the  period  of  increased  response  to  heat,  in 
both  cases  there  comes  a  period  of  quiescence,  in  which  there  is  no 
response  whatever  to  applications  of  intense  cold,  even  that  produced 
by  the  evaporation  of  a  spray  of  ethyl  or  methyl  chloride — L  e.,  the 
sensory  function  of  tlic  jjulp  is  paralyzed. 

'  American  System  of  Dentistry,  vol.  i. 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP         403 

These  are  the  available  siihjective  eviflences  of  the  anatomical  con- 
dition of  the  pulp;  while  thev  indicate  with  a  decree  of  accuracy,  useful 
in  clinical  work,  the  alterations  in  the  pulp,  the  exact  relations  between 
the  reactions  and  the  morbid  anatomy  of  the  organ  are  not  entirely 
clear.  In  the  light  of  personal  knowledge  it  is  assumed  that,  in  conse- 
quence of  the  loss  of  the  normal  protective  covering  of  the  pulj),  its 
sensory  and  perhaps  vasomotor  nerve  fibers  become  stimulated,  over- 
stimulated,  irritated,  then  paralyzed  by  thermal  stimuli  in  the  progress 
of  caries.  The  bloodvessels,  which  retained  their  tonus  up  to  a  certain 
point,  suffer  vasomotor  irritation;  next,  paralysis  leading  to  their  dila- 
tation and  to  the  throbbing  pain.  Later,  even  change  of  posture  is 
sufficient  to  cause  distention  of  the  paralyzed  vessels,  hence  pain  in 
resuming  the  reclining  position.  vStimulation  by  cold,  until  the  later 
stages,  causes  a  sharp,  continuous  pain,  ascribed  to  the  paroxysmal 
contraction  of  the  vessels;  although  unquestionably  specific,  sensory- 
nerve  reaction  is  involved.  In  the  stages  of  paralysis  heat  causes 
further  distention  of  the  vessels,  and,  if  adventitious  gases  be  present, 
causes  their  expansion  with  pressure  upon  nerve  filaments. 

The  decreasing  and  delayed  response  to  thermal  stimuli  must  be 
referred  to  three  sources:  (1)  An  increase  in  the  non-conducting  cover- 
ing of  the  pulp— i.  e.,  a  lessening  of  the  amount  of  the  fluid  contents 
of  the  dentinal  tubuli  and  a  thickening  of  the  dentinal  walls,  which 
necessarily  implies  a  recession  of  the  pnlp  from  its  normal  position; 

(2)  to  degeneration    of   the   sensory-nerve    fibers    themselves;    and 

(3)  changes  in  the  walls  of  or  about  the  bloodvessels,  which  check 
vasomotor  response  and  changes  in  the  caliber  of  the  vessels.  These 
three  classes  of  reactions  still  further  emphasize  the  division  of  the  pulp 
diseases  into  two  types,  the  acute  and  chronic;  the  first  class  of  reac- 
tion is  associated  with  the  acute  destructive  diseases;  the  second,  with 
the  chronic  constructive  but  dem-nerative  conditions. 


CONSTRUCTIVE  DISEASES  OF  THE   DENTAL  PULP. 

The  constructive  diseases  of  the  dental  pulp  include  all  the  secondary 
dentine  formations,  tubular  calcification,  the  formation  of  pulp 
nodules,  and  calcareous  degeneration  of  the  pulp. 

Tubular  Calcification. — Definition. — By  tubular  calcification,  or,  to 
express  the  coiulition  more  accurately,  tubular  dentinification,  is 
meant  the  change  that  occurs  in  the  dentine  which  leads  to  an  oblit- 


404  DISEASES  OF  THE  DENTAL  PULP 

eratioii  of  the  dentinal  tubuli  by  deposition  of  dentinal  material  along 
the  inside  of  the  walls  of  the  tubules,  with  a  corresponding  atrophy 
of  the  fibrils.  It  is  a  sclerosis  of  dentine  analogous  to  osteo- 
sclerosis. 

Causes  and  Occurrence. — The  apparent  cause  is  a  mild  degree  of 
irritation,  not  passing  the  stage  inducing  constructive  metamorphosis, 
and  apparently  caused  by  direct  irritation  of  the  fibrils,  more  par- 
ticularly through  the  action  of  thermal  shock,  brushing  or  mastica- 
tion, or  action  of  acids.  It  occurs  in  the  course  of  mechanical 
abrasion  and  erosion  of  the  teeth,  under  metallic  fillings,  and 
probably  a  modification  of  the  process  precedes  the  slow  invasion  of 
dental  caries.  It  begins  at  once  the  enamel  is  removed  from  the 
dentine  at  any  point  and  the  dentine  subjected  to  irritation,  showing 
it  to  be  due  to  a  stimulation  of  the  whole  odontoblastic  cell  (including 
its  fibrillar  prolongation).  It  occurs  in  some  degree  as  a  normal  vital 
change  due  to  age,  and  is  common  in  persons  who  are  victims  of  the 
ffoutv  or  rheumatic  diathesis. 

Pathology. — The  fibril  is  lessened  in  diameter  as  the  lumen  of  the 
tubule  becomes  smaller.  There  is  sometimes  an  increased,  but  more 
often  a  lessened,  sensitivity  of  the  dentine. 

Other  phases  of  the  condition  are  discussed  under  transparency  of 
the  dentine,  to  which  the  disease  corresponds.     (See  p.  341.) 

The  altered  dentine  becomes  translucent,  acquiring  a  horn-like 
appearance,  and,  usually,  secondary  dentine  formation  begins  coinci- 
dently  with  it.  Andrews  claims  that  granules  of  calcified  matter  are 
pushed  into  the  fibrillse  by  the  odontoblasts  and  deposited  along  the 
inner  wall  of  the  tubule,  even  to  obliteration  of  them.  These  granules 
give  the  color  to  abraded  dentine  in  the  region  of  the  pulp  cavity. 

Tubular  calcification  is,  for  the  most  part,  to  be  regarded  in  the 
light  of  an  effect  due  to  a  physiological  process.  It  may  be  regarded 
as  a  physiological  barrier  erected  against  the  progress  of  caries,  ero- 
sion, or  abrasion,  threatening  the  invasion  of  the  pulp.  While  it 
delays  the  disintegration  of  the  tissue,  it  does  not  prevent  it.  In  the 
cases  due  to  age  or  the  irritants  produced  by  goutiness,  it  is  probably 
a  local  expression  of  a  general  sclerotic  change,  the  intercellular  sub- 
stance (tubule  wall)  being  formed  at  the  expense  of  the  cellular 
(fibrilla).  In  senility  the  change  in  the  dentine  may  cause  the  teeth 
to  be  almost  traiisj)ar('nt.     It  requires  no  treatment. 

Secondary  Dentine. — Definition. — By  secondary  dentine  is  meant  a 
deposit  of  dentine  upon  the  wall  of  the  pulp  chamber,  as  the  result 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP         40.J 


of  pulj)  stimulation  after  the  pulp  has  enjoyed  a  {)hysiological  period 
of  rest  from  dentine  formation.     It  is  always  attached  to  the  dentine. 


Fir..  334 


Fig.  335 


Sec(  Hillary  dentine 
formed  after  exposure 
of  i)ulp  by  fracture  dur- 
ing extraction.    (Tomes.) 

Fig.  336 


Bicuspid  in  which  a 
formation  of  secondary 
dentine  has  failed  to  ob- 
viate perforation  of  the 
pulp  cavity  by  resorp- 
tion.    (Tomes.) 


Harding's  case  of  united  fracture.   The  uniting  material  is  of  coarse 
osseous  structure  with  numerous  lacunal  spaces.     (Tomes.) 


Fig.  337 


Causes. — The  cause  of  formation  of  secondary  dentine  is  a  stim- 
ulation of  the  pulp  to  increased  functional  activity.  This  stinuilus 
may  be  provided  by  any  constant  irritation  of 
the  dentinal  fibrils,  as,  for  example,  when  ex- 
posed at  necks  of  teeth,  upon  abraded  or 
eroded  surfaces,  or  within  cavities  of  decay. 
The  presence  of  metallic  fillings,  conductive  of 
thermal  changes,  may  provide  the  necessary 
stimulus.  Gold  crowns  upon  ground-down 
crowns  of  vital  teeth  have  a  similar  effect. 
The  slightly  irritative  effects  of  oxychloride  of 
zinc  often  produce  much  .secondary  dentine.  It 
is  a.ssociated  with  tubular  calcification.  A  pulp 
capping  may  provide  the  stimulus  and  new 
dentine  fill  the  orifice  of  exposure.  Absolute 
treatment  has   been  recorded   as  productive  of 


l",lasf  ic  layer  of  calcific 
material  formed  over  an 
exposed  pulp.  (From  a 
ca.se.) 

exposure    without 
secondarv  dentine. 


406 


DISEASES  OF  THE  DENTAL  PULP 


In  two  cases  described  by  Charles  Tomes,  pulps  widely  exposed 
by  fracture  of  crowns  during  extraction  covered  themselves  com- 
pletely in.  The  histological  record,  as  seen  in  the  photomicrograph, 
demonstrated  that  a  plastic  exudate  was  first  exuded,  which  later 
calcified  as  an  amorphous  mass. 

Next  an  irregular  lamina  was  formed,  and  lastly,  dentine  containing 
tubules.  It  is  to  be  inferred  that  both  the  pulp  and  its  odontoblasts 
may  take  part  in  the  process  (Fig.  334). 


Fig.  338 


Fig.  339 


Fig.  3.38. — Secondary  dentine  filling  the  pulp  ohamber  in  a  case  of  abra.sion  of  a  cuspid  tooth: 
a,  portion  lo.st  by  abrasion;  c,  abraded  surface;  d,  secondary  dentine,  filling  a  i)ortion  of  the  pulp 
chamber,  and  acting  as  a  protection  to  the  pulp;  e,  slender  i)oint  of  the  pulp — irregular  deposits 
are  seen  on  the  walls  of  tlie  pulp  chamber,  as  at  /,"  a,  cylindrical  calcifications  in  the  root  portion 
of  tlie  pulp  chamber. 

Fig.  3.39. — Secondary  dentine  from  the  same  specimen  as  Fig.  338,  magnified  sufficiently  to 
sliow  the  difference  in  primary  and  .secondary  tissue:  a,  abraded  surface  crown;  6,  secondary 
dentine;  c,  primary  dentine;  d,  junction  of  primary  with  secondary  dentine;  e,  remains  of  i)ulp 
tissue;  /,  small  oval  masses  of  calcific  material.     (Black.) 

I  have  seen  one  case  in  which  a  wide  exposure  had  been  covered  in 
sufficiently  to  ena})le  nie  to  gently  iiitlcnt  the  covering,  which  was 
convex,  with  a  ball  l)urnisher.  U})on  removal  of  the  instrnnient  it 
resumed  its  original  shape,  owing  to  its  elasticity.  The  periphery  of  the 
original  exposure  was  clearly  defined  (Fig.  337).  Age  seems  to  be 
a  cause  of  general  secondary  dentine  formation,  but  no  doubt  certain 
forms  of  irritation  are  introduced  competent  to  produce  the  changes. 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP         -J07 

At  times  reHex  irritation  seems  to  l)e  a  competent  cause,  as  in  cases  of 
partial  abrasion  the  unworn  teeth  may  be  affected  in  equal  degree 
with  th(*  worn  ones. 

Pathology  and  Morbid  Anatomy. — The  formation  is  usuallv  noted 
opposite  to  some  area  of  injury,  and  maybe  distinguished  from  normal 
dentine  by  its  translucency,  or  sometimes  by  its  color,  which  may  be 
a  light  brown.  The  deposit  may  be  of  fairly  regular  or  irregular 
distribution,  and  even  tumors  attached  to  the  dentine  have  been 
described  (Figs.  336  and  340). 

Black  has  shown  that  in  the  deposits  against  normal  dentine  the 
first-formed  portion  contains  an  almost  normal  number  of  tubules, 
but  their  direction  is  sharply  changed.  As  the  deposits  become  thicker 
the  tubules  become  fewer,  and  finally  the  dentine  becomes  amor- 
phous in  character  (Fig.  343). 

Black  relates  these  appearances  with  the  gradual  atrophy  and  dis- 
appearance of  the  odontoblasts.  As  tiie  pulp  l)ecomes  smaller  it 
also  necessarily  undergoes  atrophy. 

Hopewell-Smith,  treating  of  secondary  dentine  under  the  title  of 
"Adventitious  Dentine,"  mentions  several  varieties:  (1)  Fibrillar,  or 
that  containing  tube-like  markings  finer  and  less  regular  than  in 
normal  dentine.  This  would  correspond  to  that  in  Fig.  340,  h.  (2) 
Areolar,  that  containing  interglobular  spaces  formed  by  the  non-union 
of  calcospherites.  (3)  Cellular,  or  that  in  which  the  connective 
tissue  cells  of  the  pulp  remain  encapsulated  in  the  calcifying  matrix. 

(4)  Laminar,   in   which  laminated   spherites  appear    (Fig.   340,  c). 

(5)  Hyaline,  having  a  granular  or  ground-glass-like  appearance  (the 
amorphous  substance  of  Black)  (Fig.  340,/).  He  regards  the  adven- 
titious dentines  as  formed  by  pulp  cells  rather  than  by  the  odontoblasts. 

In  these  cases  the  pulp  tleposits  calcoglobulin  against  the  dentine. 
Apparently  in  some  of  Black's  cases  the  calcoglobulin  was  deposited 
about  preexisting  fibrilhe  which  contimied  to  persist  in  the  new 
formation,  the  remaining  odontoblasts  receding,  while  in  Tomes'  cases 
the  pulps  were  compelled  to  calcify  a  plastic  exudate  as  a  sort  of  basis 
for  the  begimiing  of  tubule  formation.  This  is  pr()l)ably  the  case  in 
formation  of  secondary  dentine  as  a  repair  of  exposure  under  a  eaj). 
lilack  has  shown  tliat  in  al)rasion  the  (le))osit  is  more  r(\o;ular  than  in 
caries,  without  (l(»ubt  (hie  to  the  fact  that  the  tliermal  irritation  in 
caries  is  more  irregular  than  the  irritation  of  the  fibrilhe  by  abrasion. 
A  deposit  projecting  from  any  point  about  the  pulp  cavity  side  into 
the  pulp  is  called  a  "dentinal  tumor"  (Fig.  340). 


408 


DISEASES  OF  THE  DENTAL  PULP 


The  entire  crown  may  be  removed  by  abrasion  and  yet  the  pulp 
be  protected.  In  some  cases  the  protective  action  ceases  and  the 
pulp  becomes  closely  approached  or  exposed  (Fig.  241),  probably 
due  to  a  cessation  of  secondary  dentine  formation,  the  result  of  degener- 
ation and  loss  of  odontoblasts. 

The  mode  of  deposition  upon  the  sides  of  the  canal  in  abrasion, 
shown  by  Fig.  338,  is  quite  characteristic. 

Fig.  340 


Dentinal  tumor  within  pulp  chamber:  A,  diagram  of  the  tooth,  with  dotted  line  showing  the 
position  of  the  section  B.  In  B  the  pulp  chamber  is  shown  in  section,  nearly  natural  size,  show- 
ing tlie  tumor  within.  C  is  an  illustration  of  the  tissue  of  the  tumor;  a,  a,  the  primary  dentine; 
/*,  irregular  tubules  connecting  the  newgrowth  with  the  primary  dentine — most  of  these  are  ver.y 
(lark  and  irregular;  c,  a  calcospherite  included  in  the  mass;  d,  apparently  a  bloodvessel  calcified; 
n,  calcified  tissue;  f,  a  finely  granular  mass;  g,  a  .spur  of  very  transparent  dentine.  Dentinal 
tubules  appear  at  h,  h.     (Black.) 

Deposits  in  canals  may  occur,  lessening  their  lumen  and  increasing 
the  difficulty  of  canal  exploration  (Fig.  330). 

"Secondary  growths  in  cases  of  abrasion  are  not  confined  alone  to 
the  abraded  teeth,  but  other  teeth  which  have  escaped  wear  may  be 
affected  in  equal  degree.  In  all  of  these  cases  there  is  direct  evidence 
that  the  odontoblastic  layer  has  been  stimulated  to  increased  activity 
ill  id  ])roduced  the  regular  secondary  deposition.'"  (See  Reflex  Hyper- 
ciiiiii  of  the  Pulp.) 


*  Black,  American  System  of  Dentistry,  vol.  i. 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP 


Am 


Secondary  dentine  is  often  accompanied  by  other  coiistnictive 
changes  in  the  pnlp — i.  e.,  pulp  nodules  and  calcareous  degeneration 
(Figs.  342  and  348). 

Miller  has  shown  that  dentine  resorption  by  the  pulp  may  be 
repaired  by  a  new  deposit  of  secondary  dentine,  which  Hopewell- 
Smith  has  shown  to  be  of  the  nature  of  cementum  (Fig.  361). 

Tomes*  describes  and  illustrates  a  peculiar  case  of  united  fracture 
occurring  in  the  practice  of  Mr.  Harding.  In  an  incisor  an  oblique 
fracture  occurred  which  entirely  separated  the  fractured  segment, 
yet  a  plastic  exudate  from  the  pulp  occurred  which,  when  calcified, 
attached  it  to  the  fixed  portion  of  the  tooth.  The  new  formation 
did  not  resemble  dentine  (Fig.  335). 


Fig.  341 


Fin.  342 


Fig  341. — Illustration  of  the  narrowing  of  the  pulp  chamber  in  a  molar  (superior)  by  the 
deposit  of  secondary  dentine  resulting  from  abrasion,  showing  the  [lortions  of  the  c-harrtber  in 
which  the  deposit  usually  occurs.  The  light-shaded  portion  (ft)  ."iliows  tlie  original  dimensions  of 
the  chand)er,  which,  in  this  instance,  seem  to  have  been  pretty  large;  n,  a  point  of  deep  abrasion; 
c,  r,  remaining  pulp  chamber,  which  it  mostly  filled  with  irregular  mas.ses;  </,  one  of  the  root 
canals.  It  will  be  ob.served  that  tlie  narrowing  of  tlie  root  canal  is  within  the  original  pulp 
chamber.     (Black.) 

Fig.  342. — P.  D.,  primary  dentine;  S.  D.,  secondary  dentine;  P,  i)ulp  chamber;  D,  nodules. 

Fig.  266  illustrates  a  case  of  repair  of  an  incisor  fractured  at  a 
point  well  up  beneath  the  gum,  a  condition  reasonably  in.suring 
asepsis.  A  firm  reattachment  occurreil.  I  have  seen  such  a  fracture 
which  resulted  in  ])ulp  death  and  the  coronal  portion  remained  )'// 
situ  for  two  years  (according  to  the  patient).  This  would  give  time 
for  such  a  plastic  exudate  to  form.  In  another  case  I  was  compelled 
to  remove  a  pulp  for  hyperemia  two  months  after  a  fall  fractured  a 
tooth  in  this  location. 

Kirk-  records  a  case  of  immediate  re])IautatIon  in  early  life,  followed 
in   old  age  by  root  resorption.     The  tooth  when  extracted  contained 


'  Dental  Surgery. 


-  Proceedings  of  the  .■\cademy  of  Stomatology,  1902. 


410 


DISEASES  OF  THE  DENTAL  PULP 


secondary  dentine,  which  could  only  have  formed  as  the  result  of  a 
reattachment  of  the  pulp. 

W.  H.  Trueman^  reported  that  hypersensitive  dentine  was  noted 
some  years  after  a  replantation  under  similar  conditions. 

Osteodentine. — Tomes  states  that  secondary  dentinal  deposits  may 
assume  the  character  of  osteodentine,  a  form  of  dentine  found  in  the 
teeth  of  some  animals,  in  which  the  tissue  presents  combined  char- 
acteristics of  both  bone  and  dentine.  He  cites  the  example  also  that 
elephants'  tusks  are  frequently  repaired  with  osteodentine  after  injury. 

Fig.  343 


Calcification  or  clepf)sit  of  secondary  dentine,  resulting  from  caries  of  an  incisor:  A,  diagram 
of  section  of  incisor,  showing  caries  at  a,  and  secondary  dentine  at  b.  B,  illustration  magni- 
fied 200  diameters,  to  show  the  tissue  of  the  secondary  dentine:  a,  pulp  chamber;  b,  b,  secondary 
dentine;  c,  primary  dentine.  It  will  be  noticed  that  the  dentinal  tubes  in  the  secondary  dentine 
gradually  disappear,  giving  place  to  a  clear  calcification.      (Black.) 


The  specimen  illustrated  (Fig.  344)  was  taken  from  a  case  in  which 
the  coronal  portion  of  the  pulp  chamber  was  almost  obliterated  by 
a  deposit  of  secondary  dentine.  Probably  some  of  the  pulp  cells 
have  taken  on  the  characteristics  of  osteoblasts.  Tissue  resembling 
cementum  seems  to  be  frequently  found  as  a  tissue  of  repair  (Fig.  3()5). 
Results  of  Secondary  Dentine.  -The  formation  of  large  masses  of 
secondary  dentine  iiiKjiiestionubly  ))rings  about  a  degenerative  con- 
dition of  the  j)ulp  which  may  become  a  cause  of  neuralgia.     The  pulp 

'  Proceedings  of  the  Academy  of  Stomatology,  1902. 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP 


411 


may  (lie,  and,  l)ec()iiiiiig  iiifrctcd,  may  produce  pericemental  irritation. 
In  one  case  seen  the  secondary  deposit  in  the  j)ul{)  chamber  had 
separated  the  canal  filaments  of  the  pvdp  of  a  multirooted  tooth  into 
independent  pulps,  one  of  which  was  dead  and  the  others  alive  and 
undergoing  degeneration.  The  specific  symptoms  were  those  of  peri- 
cementitis— i.  e.,  elongation  and  tenderness  to  percussion. 

In  another  case  of  a  first  upper  bicuspid  the  lingual  filament 
was  perfectly  covered  in  and  vital.  The  buccal  filament,  likewise 
enclosed  and  isolated,  contained  an  abscess  within  the  pulp. 


Fig.  344 


Osteodentine:  .4,  outline  of  incisor,  showing  a  narrowing  of  the  root  canal  at  h  by  a  deposit 
of  osteodentine.  B.  illustration  of  the  tissue:  a.  primary  dentine;  h,  line  of  the  beginning  of  a 
growth  of  secondary  dentine;  c,  secondary  dentine;  d,  layer  of  granular  matter;  e,  osteodentine; 
this  has  the  lacuna;  at  p  and  dentinal  tubes  at  k;  f  seems  to  be  the  surface  of  ttie  osseous 
deposit;  i,  irregular  crystalline  deposits;  h,  the  pulp  chamber.       X   350.      (Black.) 

The  symptoms  complained  of,  however,  were  those  of  acute  peri- 
cemental irritation,  simulating  inci])ient  septic  apical  pericementitis 
(Fig.  371). 

It  has  been  shown  by  Hopewell-Smith  that  microorganisms  may 
enter  the  pidp  by  way  of  the  spaces  or  tubes  in  adventitious  dentine. 
In  Burchard's  case  a  molar  containing  a  deep  cavity  filled  with  zinc 
phosphate  gave  vague  pain,  finally  referred  to  the  tooth,  which  re- 
sponded only  faintly  to  hot  applications  and  not  at  all  to  cold  ones. 
Secondary  dentine  was  found  complicated  by  calcareous  degeneration 
— I.  e.,  a  degenerated  pulj)  was  present. 

In  certain  cases  a  deposit  extends  well  into  a  canal,  totally  obliter- 
ating it  for  much  of  its  length.     Unless  symptoms  be  present  it  may 


412  DISEASES  OF  THE  DENTAL  PULP 

ordinarily  be  left.  In  such  cases  thermal  tests  for  pulp  vitality  seem 
often  inconclusive.  The  electric  current  should  be  a  more  satisfactory 
means  of  diagnosis,  provided  the  dentine  be  moist.  Secondary 
dentine  is  sometimes  quite  hypersensitive,  as  shown  by  attempts  at 
entering  the  pulp;  in  most  cases  it  is  quite  insensitive  until  the  pulp 
is  reached.  It  is  also  difficult,  as  a  rule,  to  force  cocaine  through 
secondary  dentine,  even  with  a  compound  syringe,  and  arsenic  acts 
slowly,  though  it  devitalizes  if  the  dentine  be  sensitive.  (See  Dry 
Gangrene.) 

Treatment. — Secondary  dentine  which  has  been  regularly  deposited, 
and  particularly  in  the  canals  of  anterior  teeth,  calls  for  no  treatment. 
Should,  however,  great  hypersensitivity  of  the  dentine  and  pulp,  or 
pulp  disease,  be  evident  or  inferred  from  symptoms,  the  pulp  should 
be  removed.  This  may  involve  a  search  of  some  difficulty  and  necessi- 
tate the  removal  of  much  dentine.  The  canals  may  be  much  con- 
stricted, especially  at  that  portion  nearest  the  pulp  chamber.  The 
condition  may  be  more  or  less  complicated  by  the  presence  of  pulp 
nodules  or  calcific  degenerations  in  addition  to  the  secondary  dentine. 

Pulp  Nodules. — Definition. — Pulp  nodules  (pulp  stones,  nodular 
calcifications)  are  masses  of  more  or  less  translucent,  calcific  material, 
apparently  the  result  of  secretion,  having  a  fairly  definite  histological 
structure  differing  from  that  of  dentine,  and  occupying  a  position 
within  the  pulp  substance.  They  are  rarely  fused  with  the  dentinal 
walls  of  the  pulp  chamber,  and  then  are  included  by  formation  of 
secondary  dentine  about  them. 

Occurrence.— While  these  growths  may  occupy  the  pulp  chambers 
of  teeth  in  which  the  pulp  has  been  the  seat  of  direct  irritation,  their 
occurrence  is  by  no  means  confined  to  such  teeth.  They  are  found  not 
only  in  teeth  which  have  suffered  abrasion,  erosion,  and  slowly  pro- 
gressing caries,  but,  as  pointed  out  by  Black,  they  may,  and  frequently 
do,  form  in  other  teeth  of  the  same  denture  which  are  not  directly 
involved  in  the  irritation.  This  investigator  notes  that  irritation  of  the 
pulp  of  one  tooth  of  a  denture  very  frequently  causes  a  general  hyper- 
esthesia of  the  pulps  of  all  of  the  teeth.  This  is  particularly  notable 
in  the  type  of  persons  classed  as  neuralgic.  It  is  also  common  in 
pe^rsons  of  the  hyperacid  diathesis.  Nodules  are  found  much  more 
frequently  in  the  teeth  of  middle-aged  persons  than  in  those  of  youth, 
although  they  may  be  present  as  early  as  the  fifteenth  year.  They 
occur  more  frequently  multiple  than  single.  Some  of  the  larger 
nodules  are  evidently  formed  by  the  coalescence  of  smaller  ones. 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


413 


Pathology  and  Morbid  Anatomy. — ^The  structure  of  pulp  nodules  does 
not  resemble  that  of  dentine;  they  possess  about  the  same  degree  of 
translucency  and  hardness  as  secondary  dentine.  Outwardly  they 
may  assume  almost  any  form;  they  range  in  size  from  minute  bodies 
to  a  size  sufficient  to  almost  obliterate  the  pulp  (Figs.  342  and  348). 

Fig.  345 


PN 


A  pulp  nodule  fused  to  the  parietes  of  a  pulp  cavity.     Prepared  by  grinding:     PN,  pulp  nodule; 
Z),  dentine  of  the  tooth.      X  15.     From  section  by  J.  F.  Colyer.     (Hopewell-Smith.) 


A  section  of  a  nodule  exhibits  the  jiresence  of  a  number  of  concen- 
trically laminated  bodies,  recognizable  as  hardened  calcospherites. 
Black  found  them  to  rarely  make  up  any  considerable  portion  of  the 
bulk  of  the  nodule.  The  remainder  of  the  nodule  is  made  iij)  of 
structureless  material  which  may  contain  a  few  fine  tubes. 

He  also  found  deposits  in  the  pulp  which  throw  light  upon  the 


414 


DISEASES  OF  THE  DENTAL  PULP 


possible  origin  of  nodules  in  some  cases,  and  to  some  extent  upon 
the  conditions  under  which  they  may  be  formed.  In  the  pulp  of 
a  second  molar  of  a  girl  aged  fifteen,  in  which  there  had  been  decided 
subjective  evidences  of  pulpitis  recurring  at  intervals  for  a  period 


Fig.  346 


Section  of  a  pulp  nodule,  showing  many  calcospherites,  as  pointed  out  by  a,  a.     (Black.) 

of  two  months,  he  found  a  mass  representing  a  pulp  nodule  in  its 
soft  state.  "About  one-half  of  the  coronal  portion  of  the  pulp  was 
involved  in  the  inflammation ;  lying  a  little  inside  of  the  layer  of  odonto- 
blasts were  several  masses  similar  to  Fig.  347,  having  globular  forms 


Fig,  347 


Deposit  of  calcoKlobuliii  within  the  tissues  of  an  inflamed  pul|).      (Black.) 

in  fhcir  mass  or  attached  to  their  margins.  The  globular  bodies 
present  th(!  huniiiated  appearance  of  calcospherites."  These  masses 
may  in  all  j^robability  be  interpreted  as  intermediate  })roducts  in  the 
formation  of  nodules ;  they  have  not  yet  become  calcified. 


COXSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP 


415 


A  small  nodule  may  be  made  up  of  laminated,  structureless  material 
the  lamina'  being  arranged  al)out  a  central  nucleus,  the  nature  of 
which  i.s  not  c-lear,  but  may  po.s.sil)ly  be  calcified  dead  cells  (Fig.  349). 

The  conchtions  of  calcification  of  nodules  are  not  definitely  known. 
Hopewell-Smith  considers  that  they  are  deposited  by  the  pulp  cells  as 
a  secretion  about  themselves,  and  that  the  cells  are  later  obliterated 
or  may  persist  in  situ  (Fig.  350).  He  also  describes  and  ilhistrates 
a  case  of  a  nodule  wliich  had  witliin  it  a  pulj)  cavity  containing  pulp 
tissue. 


5 


Calcification  of  the  dental  pulp:  At  A  is  shown  the  outline  of  a  lower  molar  with  a  caWty 
at  6.  The  pulp  chamber  is  much  reduced  in  size  and  filled  with  calcific  material,  as  shown 
in  B.  a,  a,  large  granular  mass  of  calcific  material,  which  is  very  transparent  but  finely 
granular.  A  very  few  irregular  lines  are  seen  in  the  centre,  which  slightly  resemble  tlentinal 
tubes;  6,  an  erratic  growth  of  irregularly  formed  and  unusually  transparent  dentine;  c,  line  of 
the  growth  of  dentine  from  the  floor  of  the  pulp  chamber — the  growth  from  other  directions 
is  so  perfectly  regular  as  to  leave  no  markings;  d,  margin  of  the  cavity  of  decay;  e,  a  bundle 
of  cylindrical  forms  of  calcific  material  extending  down  into  the  root  canal.  These  extended 
to  the  apex  of  the  root.      (Black.) 

Pul})  nodules  occur,  as  a  rule,  in  the  better  grades  of  teeth  which 
show  constructive  tendencies  upon  the  part  of  the  pulp. 

It  is  possible  that  in  these  pul{)s  the  pulp  cells  under  conditions  of 
irritation  secrete  calcoglobulin,  which  in  part  is  developed  into  .spherites 
and  in  part  remains  without  definite  histological  characteristics.  The 
masses  are  probably  calcified  after  their  deposition.  Whatever  the 
origin  of  the  masses — by  cell  secretion  or  otherwise — the  histological 
record  intlicates  a  gratlual  increase  in  the  size  of  the  deposit.     Pressure 


416  DISEASES  OF  THE  DENTAL  PULP 

upon  the  nerves  results  in  irritation.  Pulp  nodules  are  usually  found 
in  the  coronal  portion  of  the  pulp,  but  sometimes  exist  in  the  root 
portions,  either  free  or  embedded  in  secondary  dentine.  If  they 
obstruct  the  lumen  of  the  canal  they  cause  interference  with  the 
circulation  and  nerve  tissue  and  may  produce  great  pain.  As  in 
the  case  of  secondary  dentine,  nodules  may  be  produced  by  reflex 
hyperemia,  as  they  are  quite  frequently  found  in  teeth  near  to  an 
impacted  tooth. 

Symptoms. — Multiple  nodules  may  exist  in  a  dental  pulp  and  give 
rise  to  no  evident  symptoms  whatever,  as  is  shown  by  their  presence 

Fig.  349 


A  pulp  nodule  isolated  from  the  pulp.  Shows  its  central  nuclear  formation  and  its  concentric 
lamination.  Prepared  by  grinding.  X  50.  From  collection  of  G.  W.  Watson.  (Hopewell- 
Smith.) 

ill  extracted  teeth,  many  of  them  free  from  caries,  and  in  which  there 
was  no  history  of  pain.  On  the  contrary,  the  pulp  of  a  tooth  may 
be  the  seat  of  intractable  pain  without  a  depth  of  carious  invasion 
which  would  lead  to  the  inference  of  acute  pulp  disease;  and  relief 
(^nly  be  secured  through  divitalization  of  the  pulp,  which  upon  exami- 
nation may  reveal  a  small  pulp  nodule. 

The  .symptoms  attendant  upon  the  presence  of  nodules,  so  far  as 
they  can  be  made  out,  appear  to  be  of  two  tyf)cs — those  associated 
with  small  and  tlx^se  with  extensive  deposits.  Reflex  {)uin  is  the 
connnon  associate  of  both. 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP         417 

Small  Deposits. — While  it  is  true  that  pulp  nodules  may  some- 
times exist  in  apparently  sound  teeth  without  intlucing  pain,  yet  the 
pulps  of  teeth  containing  them  become  excessively  hyperesthetic 
under  what  are  ordinarily  mild  sources  of  irritation.  This  is  mani- 
fested, first,  through  the  contents  of  the  dentinal  tubuli;  the  dentine 
becomes  exquisitely  sensitive  and  cool  water  directed  into  a  shallow 
cavity  produces  a  paroxysmal  and  excruciatingly  painful  response 
from  the  pulp.  In  the  absence  of  direct,  extraneous  irritation  of  the 
pulp,  the  dental  symptoms  may  be  absent,  but  a  persistent  neuralgia 
may  be  located  at  some  distant  point.     Pain  in  the  ear  is  a  frequent 

Fig.  350 


PN 


M  N 


MN 


Tlie  fonnation  of  the  pulp  nodule.  I'repuied  by. Mi.  Hopewell-Smith's  proces.*.  P  .V,  puip 
nodules;  M  N,  medullated  nerve  bundles;  P,  pulp  tissue;  C,  capillary.  X  230.  (Hopewell- 
Smith.) 

symptom.  Occasionally  an  obstinate  scalp  neuralgia,  with  the  exist- 
ence of  a  hyperesthetic  .spot,  appears.  Pain  in  the  eye,  with  tenderness 
over  the  supra-orbital  foramen,  is  also  common.  Guilford'  has 
reported  a  ca.se  of  tic  douloureux  of  two  years'  standing,  the  result  of 
pulp  nodules.  The  pain  may  be  recurrent  or  persistent.  If,  in  the 
absence  of  a  more  probable  explanation  of  the  pain,  a  pulj)  nodule  be 
suspected,  and  arsenical  applications  be  made  to  devitalize  the  pulp,  it 
is  found  that  not  only  is  inten.se  pain  cau.sed,  but  examination  after 
from  forty-eight  to  seventy-two  hours  shows  the  pulp  to  be  still  vital 

'  Private  communication. 

27 


418  DISEASES  OF  THE  DEXTAL  PULP 

and  h^-persensitive ;  and,  in  order  to  effect  its  destruction,  repeated 
applications  and  large  doses  of  arsenic  must  be  used.  Cocaine 
introduced  bv  cataphoresis  is  also  apt  to  be  slow  in  action. 

Large  Deposits. — In  extensive  deposits  of  pulp  nodules  the  dentine 
may  be  almost  devoid  of  sensation,  and  applications  of  heat  or  cold, 
even  in  large  cavities,  may  be  followed  by  delayed  and  faint  pulp 
response.  Such  cases,  however,  commonly  give  a  history  of  reflex 
neuralgia  and  vague  dental  pains  extending  over  a  period,  it  may  be, 
of  years.     With  some  large  deposit  the  pain  may  be  exquisite 

Diagnosis. — Their  diagnosis  by  means  of  the  a:-rays  is  positive  (Figs. 
351  and  352),  but  their  diagnosis  by  symptoms  may  only  be  inferential 
and  confirmation  be  lacking  until  after  devitalization  of  the  pulp  and 
the  finding  of  the  pulp  nodules  in  its  substance. 

The  tardy  action  of  arsenic  is  also  observed  in  the  cases  of  large 
deposits,  it  being  frequently  necessary  to  devitalize  the  pulp  piece- 
meal, and  sometimes  the  arsenic  will  hardly  be  tolerated  at  all. 

Fig.  351  Fig.  352 


Pulp  nodules  in  the  radicular  and  coronal  portions  of  the  canal.      (Skiagraphs  by  Price.') 

Treatment. — Pulps  inferred  or  shown  by  x-rays  to  contain  nodules 
should  be  removed.  If  the  cataphoric  apparatus  or  compound 
syringe  be  at  hand  it  may  be  used  to  benumb  the  pulp  by  cocaine; 
at  least,  sufficiently  for  the  removal  of  the  nodule.  If  desired,  the 
remainder  of  the  pulp  may  be  anesthetized  by  the  same  means  or 
ordinary  cocaine  pressure  anesthesia  and  removed.  The  Ijloodletting 
attendant  upon  removal  of  the  bulb  of  the  pulp  usually  permits  an 
arsenical  application  for  devitalization  of  the  remainder  of  the  pulp 
to  be  painlessly  made,  but  this  is  not  always  the  case. 

The  same  result  may  be  attained  by  drilling  open  the  pulp  cavity 
while  the  patient  is  under  the  influence  of  nitrous  oxide  gas  or  somno- 
form,  or,  possil^ly,  intra-alveolar  injection  of  cocaine. 

At  times  aresnic  may  be  apj)lied  to  the  pulpal  wall  of  the  cavity, 

'  Items  of  Interest,  1901. 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP         419 

if  one  exist,  or  in  a  specially  j)r('j)are(l  pocket,  without  production  of 
painful  reaction. 

After  forty-ei<,'ht  hours  a  portion  of  flentine  is  to  be  removerl  and 
a  stronger  apj)lication  made.  When  the  pulp  is  clo.sely  approached, 
the  arsenic  is  to  he  left  a  week  or  longer  in  position,  when,  as  a  rule, 
the  nodule  may  he  removed.  Another  application  may  then  he  left 
in  position  for  a  week  or  longer  to  insure  devitalization. 

If,  after  devitalization,  the  nodule  or  calcific  degeneration  he  found 
as  a  spicuhir  <lc|)()sit  in  the  mouth  of  the  canal,  it  may  usually  he 
removed  by  tciising  it  from  side  to  side,  first  soaking  the  part  with 
a  sodium  dioxide  solution,  or  50  per  cent,  sulphuric  acid,  which  cjuickly 
destroys  the  organic  matter  of  the  pulp. 

Pericemental  reactions  are  quite  apt  to  follow  the  removal  of  such 
pulps.  This  result  is  best  obviated  by  awaiting  the  thorough  death 
of  the  pulp  filaments  before  attempting  their  removal. 

If  such  reaction  arise,  strong  sedatives,  such  as  menthol  solutions, 
are  to  be  applied  on  cotton  as  root-canal  dressings,  and  counter- 
irritants  are  to  be  a})plied  to  the  gum.  (See  Aseptic  Apical  Peri- 
cementitis.) 

Cacific  Degeneration  of  the  Pulp. — By  a  calcific  degeneration  is 
meant  the  infiltration  of  inorganic  matter  derived  from  the  lymph  into 
tissue  which  is  dead  or  undergoing  degeneration.  It  occurs  in  any 
part  of  the  body  in  which  the  necessary  conditions  are  present.  (See 
p.  .SO.) 

Causes  and  Pathology. — The  conditions  apparently  necessary  for 
the  production  of  calcific  degeneration  are  those  which  occur  in  a 
semistagnant  blood  current.  An  acid  reaction  occurs  owing  to 
the  presence  of  an  excess  of  carbon  dioxide.  The  albuminous 
matter  of  the  tissue  undergoes  degenerative  changes  owing  to  the 
faulty  nutritive  supply  and  waste  removal. 

Probably  some  cells  die.  They  or  their  constituents  have  some 
affinity  for  inorganic  .salts  which  are  taken  up  from  the  lymph.  Thus 
gradually  the  tissue  becomes  infiltrated. 

Those  causes  which  produce  a  sufficient  degeneration  of  pulp  tissue 
to  induce  the  above  process  are:  (1)  the  puly)  exhaustion  due  to  the 
formation  of  secondary  dentine  or  pulp  nodules;  (2)  continued  hyper- 
emia or  chronic  inflannnation  in  which  venous  hyperemia  plays  a 
part. 

Pathology  and  Morbid  Anatomy. — The  calcic  material,  unlike  the 
cases  of  nodular  calcification,  encloses  the  anatomical  elements  of  a 


420 


DISEASES  OF  THE  DENTAL  PULP 


pulp  in  process  of  degeneration  in  a  mass  produced  by  deposition, 
not  secretion.  In  the  root  portions  of  pulps  in  which  fibrous 
elements  have  become  pronounced  the  calcification  may  be  tubular 
or  cylindrical  in  character,  the  nature  of  the  calcareous  masses 
being  apparently  a  deposition  about  and  along  the  fibers  (Fig.  353). 

The  pulps  are,  of  course,  living.  There  is  a  comparative  absence 
of  cellular  elements  in  the  pulp — i.  e.,  they  have  atrophied,  degen- 
erated, and  been  absorbed.  Upon  optical  examination  the  masses 
are  seen  to  be  opaque,  are  brittle,  and  decidedly  unlike  pulp  nodules 
in  form. 

Another  evidence  of  the  cellular  degeneration  is  seen  in  the  great 
ease  with  which  such  pulps  are  removed  after  devitalization,  even 
the  most  minute  apical  portions  freely  coming  away  after  slightly 

Fig.  353 


A,  outline  of  a  lower  molar,  with  a  large  carious  cavity  at  a;  b,  pulp  chamber;  the  shaded 
portion,  c,  was  occupied  by  cylindrical  calcifications.  B,  cylindrical  calcifications.  X  100. 
(Black.) 

catching  a  hook  in  the  pulp,  i.  e.,  the  usual  odontoblastic  attachment 
to  the  dentine  is  not  present.  When  extracted  these  pulps  have  a 
granuhir  feel  to  the  fingers,  and  when  dry  may  be  quite  stiff  (Fig.  354). 

Symptoms. — Degenerations  of  the  pulp,  as  a  rule,  present  symptoms 
of  reflex  pain,  vaguely  referred  to  other  parts.  The  response  to  hot 
applications  is  usually  greater  than  that  to  cold  ones,  and  both  are 
delayed — i.  e.,  five  seconds  or  more  may  elapse  before  pain  follows 
a  severe  test  like  the  intensely  cold  spray  of  ethyl  chloride  or  a  hot 
burnisher  or  blast  of  hot  air.  At  times  with  an  open  pulp  chamber 
the  symptoms  of  chronic  pulp  inflammation  are  ol>tained.  There 
may  be  a  y)ainful  reaction  to  arsenic  applied  to  the  pulp. 

Diagnosis  and  Treatment. — The  a;-rays  should  aft'ord  a  positive 
fliagnosis,  but  in  their  absence  the  diagnosis,  apart  from  the  inference 
from  the  .sym[)toms,  is  a  postmortem  one.     In  cases  warranting  the 


CONSTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP 


421 


Fig.  354 


interference,  in  which  thene  is  a  delayed  response  to  intense  thermal 
tests  applied  to  a  filling  or  a  clean  pulpal  wall,  the  dentine  over  the 
pulp  should  be  removed  and  the  pulp  devitalized.  Upon  removal 
of  the  pulp  it  may  be  found  to  contain  one  or  more  large  or  many 
granular  masses. 

Fig.  354  illustrates  a  case  discovered  upon  fracture  of  a  molar 
during  the  operation  of  extraction.  In  another  case  the  pulp  was 
slightly  bendable  when  extracted,  but  after 
drying  for  a  half-hour  became  at  its  apical 
end  of  needle-like  sharpness  and  stiffness. 
It  was  filled  with  calcific  granules. 

The  constructive  diseases  of  the  pulp  are 
an  evidence  of  an  attempt  upon  the  part  of 
the  pulp  to  protect  itself;  but  with  the 
exception,  perhaps,  of  a  very  regularly 
deposited  secondary  dentine  the  effects 
react  upon  the  pulp  itself,  causing  its 
destruction.  To  what  extent,  therefore, 
secondary  dentine  is  beneficial  is  an  open 
question.  Evidences  of  constructive  action,  upon  the  part  of  the 
pulp,  may  occasionally  be  noted  in  the  temporary  teeth — e.  g., 
secondary  dentine  following  deep  abrasion. 

There  do  not  seem  to  be  any  observations  as  to  the  formation  of 
nodules  or  calcific  degenerations  in  the  pulps  of  temporary  teeth,  l)ut 
there  is  no  good  reason  why  they  should  not  occur,  particularly  after 
abrasion.  The  pulp  tliseases  of  the  temporary  teeth  are  usually  of 
an  acutely  destructive  nature,  which  may  account  in  some  degree  for 
the  absence  of  reports  touching  this  subject. 


Lingual  filament  of  pulp  of 
an  upper  molar,  broken  in  ex- 
traction. The  rigidity  of  the 
filament  was  due  to  the  pres- 
ence of  calcific  granules. 


CHAPTER    XVL 

DESTRUCTIVE   DISEASES   OF  THE   DENTAL  PULP. 

This  class  of  pulp  diseases  consists  of  those  of  an  acute  character, 
although  chronic  diseases  may  arise  as  sequels  of  the  original  con- 
ditions. They  are  essentially  destructive  in  character  and  attended 
by  prompt  degeneration  of  pulp  tissues.  The  most  important, 
clinically,  are  those  having  an  evident  association  with  disorders  of 
the  bloodvessels  of  the  pulp. 

HYPEREMIA  OF  THE  PULP. 

r 
i 

Hyperemia  of  the  pulp  is  an  excess  of  blood  in  the  more  or  less 
dilated  vessels  of  that  organ.  It  is  of  two  forms:  active  or  arterial 
hyperemia,  and  venous  or  passive  hyperemia  or  congestion.  These 
two  classes  differ  in  their  probable  direct  causations  and  in 
effects. 

Active  Hyperemia  of  the  Pulp. — Definition. — Active  or  arterial 
hyperemia  of  the  pulp  is  an  excess  of  blood  in  the  dilated  arteries 
and  capillaries  of  the  pulp,  the  pulp  functions  being  increased  in  mild 
continued  cases  or  disturbed  by  a  gradual  passage  of  the  condition  into 
a  venous  hyperemia  in  more  severe  cases. 

Causes. — The  most  common  cause  of  active  hyperemia  of  the  pulp 
is  a  lessening  of  the  non-conducting  covering  of  the  organ,  enamel,  and 
dentine,  leading  to  an  increased  response  and  continued  irritation  of 
the  pulp  through  thermal  stimuli.  A  similar  condition  consists  in  the 
presence  of  large  metallic  fillings  in  close  proximity  to  the  pulp, 
through  which  abnormal  thermal  stimuli  are  received.  I'illings 
through  which  prompt  pulp  response  to  thermal  changes  are  felt  are 
a  direct  menace  to  the  continued  health  of  the  pulp.  It  is  surprising, 
however;  to  what  an  extent  the  pulp  may  protect  itself  against  such 
.stimuli  by  the  formation  of  secondary  dentine  and  tubular  calcification. 
The  vigorous  use  of  sandpaper  disks  in  finishing  large  fillings  may 
precipitate  an  attack  of  pulp  hyperemia,  but  only  if  the  pulp  is  in  a 


HYPEREMIA  OF  THE  PULP  423 

critical  condition.  The  loss  of  tooth  substance  mentioned  may  occur 
either  through  abrasion,  erosion,  fracture,  or  caries.  The  condition 
frequently  occurs  without  direct  exjK)sure  of  the  dental  pulp,  and  at 
times  when  cavities  are  relatively  shallow.  Even  the  simple  cervical 
exposure  of  dentinal  fibrilhe  may  cause  it,  but  does  not  often  do  .so. 
Septic  dentine  beneath  fillings  acts  as  a  cau.se  by  constantly  irritating 
the  dentinal  fibrillae.  The  leaving  of  septic  dentine  in  a  cavity  and 
a  firmly  placed  yet  leaking  filling  may  so  act.  Inclusion  of  saliva 
beneath  a  metal  or  gutta-percha  filling,  and  the  imperceptible  shifting 
of  a  filling  during  j)lacement,are  causes  of  septic  dentine.  Amalgam 
may  so  .shift  if  slight  yet  excessive  force  be  u.sed  in  finishing  at  the 
first  sitting.  The  sign  is  the  appearance  and  disappearance  of 
moisture  at  a  visible  margin  as  the  filling  is  moved.  This  is  often 
unobserved  unless  one  be  very  thoughtfid  of  its  possibility.  The 
cement  beneath  an  ill-fitted  crown  also  appears  to  become  saturated 
with  saliva  or  serum,  and  its  odor  indicates  septic  irritation. 

Pulp  hyperemia  may  also  be  caused  by  injury  to  the  apical  tissue 
of  a  tooth  containing  a  vital  pulp.  Malocclusion  from  any  cause, 
overfull  fillings  or  crowns,  a  blow,  or  overmalleting,  as  the  extrasion 
occurring  in  pyorrhea  alveolaris,  is  competent  to  produce  it.  An 
abscess  upon  an  adjacent  tooth  may  have  its  area  of  hyperemia 
extend  into  the  apical  tissue  of  the  tooth  adjoining,  thus  producing 
hyperemia  of  the  pulp.  A  fairly  deep  pyorrhea  p;)cket  may  fre- 
quently act  in  a  similar  manner  upon  the  pulp  of  the  tooth.  Aij 
intense  hyperemia  or  inflammation  in  the  pulp  of  one  tooth  may,  by 
reflex  action,  produce  hyperemia,  with  its  characteristic  response  to  hot 
and  cold  applications,  in  another  tooth.  It  may  occur  from  the  presence 
of  a  pulp  nodule,  or  be  due  to  the  causes  exciting  hypercementosis. 
An  aphthous  ulcer  upon  the  gum  over  a  tooth  has  produced  arterial 
hyperemia  of  the  j)ulp  by  reflex  action.  Also  an  ulcerated  alveolar 
process  resulting  from  infected  alveolus,  or  the  use  of  alveolar  forceps, 
or  even  the  regular  healing  of  an  alveolus  after  extraction,  may  cause 
it  in  a  healthy  adjoining  or  even  distant  tooth.  Also  any  irritation 
along  any  branch  of  the  fifth  nerve  or  any  of  its  terminals  may  reflexly 
induce  a  hyperemia  of  the  pulp. 

Unquestionably,  systemic  conditions,  as  malaria,  or  syphilis,  or  irri- 
tation in  another  part  of  the  body  than  that  supplied  by  the  fifth 
nerve,  as  the  uterus  or  bladder,  may  excite  pain  in  the  teeth,  which, 
if  repeated,  sooner  or  later  excites  a  hyperemia,  as  in  the  case  of  scalp 
tenderness  from  dental  disease,  and  which  will  prol)al)ly  be  tempo- 


424         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

rary,  but  may  induce  infarction.  The  mode  of  hyperemia  produc- 
tion is  probably  a  variation  in  general  nervous  tension,  or  a  general 
variation  in  blood  pressure. 

Apart  from  the  hyperemia  occurring  in  inflammation  and  that  due 
to  septic  dentine,  or  a  septic  extradental  inflammation,  it  may  be 
said  that  arterial  and  venous  hyperemia  are  mainly  due  to  non-septic 
causes,  and  even  in  septic  cases  to  be  mainly  in  itself  aseptic,  in  so  far 
as  the  pulp  is  concerned. 

Symptoms. — ^The  symptoms  of  arterial  hyperemia  vary  according  to 
the  degree  of  vascular  disturbance.  So  long  as  a  quick,  sharp  pain  is 
produced  by  contact  with  cold  or  hot  substances,  ceasing  immediately, 
and  only  reappearing  in  response  to  direct  stimuli,  no  serious  vascular 
disturbance  is  inferred;  but  when  paroxysms  of  sharp  pain,  lasting 
from  many  minutes  to  hours,  follow  upon  an  application  of  cold  to  a 
carious  cavity,  an  unbroken  enamel  surface,  a  filling,  or  an  area  of 
erosion  or  abrasion,  a  profound  disturbance  of  the  vessels  of  the 
pulp  is  indicated. 

The  pains,  in  the  absence  of  direct  irritation,  are,  as  a  rule,  but 
vaguely  located.  During  paroxysms  it  is  of  a  lancinating  character, 
and  usually  reflected  to  another  part  than  the  tooth  affected — e.  g.,  a 
sound  tooth  at  a  distance,  the  gum  between  or  above  the  teeth,  the 
ear,  the  eye,  the  supra-orbital  region,  the  infra-orbital  region,  the 
scalp,  the  chin,  the  arm,  etc. 

As  a  ride,  when  an  upper  tooth  is  affected,  the  pain  is  located  in 
the  superior  maxillary  division  of  the  fifth  nerve;  if  a  lower,  m  the 
inferior  maxillary  division.  The  pain  varies  in  intensity  from  a  vague 
uneasiness  to  an  acute  neuralgic  attack,  with  tender  spots  over  the 
point  of  emergence  of  the  nerve  tracks,  at  the  supra-orbital  and 
infra-orbital  and  mental  foramina.  The  neuralgic  pains  are  not 
always  constant;  they  may  disappear  from  the  second  or  third  division 
of   the  fifth  nerve  and  appear  in  the  first. 

The  proof  of  the  direct  connection  between  the  pulp  pain  and  the 
neuralgia  may,  in  some  cases,  be  clearly  made  out  by  the  thermal  test. 
When  a  jet  of  cool  water  is  directed  against  the  tooth  whose  pulp  is 
afi'ected,  it  may  produce,  in  addition  to  a  local  pain,  an  aggravation  of 
the  neuralgic  pains,  but  one  must  carefully  exclude  the  extradental 
causes  before  diagnosticating  a  necessity  for  interference  with  the 
tooth  tested: 

Pathology  and  Morbid  Anatomy. — The  one  distinctive  and  charac- 
teristic anatomical  condition  associated  with  active  hyperemia  is  an 


HYPEREMIA  OF  THE  PULP 


425 


irregular  dilatation  of  the  vessels  of  tlu^  pulp.'  Fig.  355  represents 
a  section  of  the  pulp  of  a  tooth  extracted  during  a  paroxysm  of  acute 
pain — "acute  paroxysms  of  pain  lasting  for  an  hour  or  more  were 
occasionally  occurring  in  consequence  of  very  trivial  changes  of 
temperature;  the  condition  had  existed  for  several  weeks."  In  some 
cases  of  a  similar  character — /.  e.,  presenting  the  same  symptoms,  hut 
extracted  during  an  interval  of  quiet — nothing  remarkable  is  pre- 
sented.    The  gradual  enlargement  of  the  veins  indicates  the  lessening 


Fig.  355 


Hyperemia  of  the  dental  pulp,  showing  the  injection  of  the  vessels:  a,  a,  membrana  eboris, 
or  layer  of  odontoblasts;  6,  h,  b,  6,  vessels  distended  with  blood;  c,  c,  c  c,  points  from  which 
the  blood  has  fallen  in  handling  the  section.     (Black.) 

outlet  at  the  apical  foramen;  or,  in  other  words,  the  beginning  and 
establishment  of  a  venous  hyperemia. 

The  most  rational  explanation  of  the  dilatation  of  the  ves.sels  is  that 
it  is  an  irregular  paralysis  of  vessel  walls — /.  e.,  of  vasomotor  nerves. 
Whether  the  more  usual  painful  responses  of  the  pulp  to  thermal 
stimuli  are  due  to  the  stimulation  of  vasodilator  fil)ers,  which  causes 
hyperemia,  is  a  matter  of  doubt;  but  the  pathological  conditions 
noted  in  pronounced  hyperemia  signify  a  paralysis  of  vasoconstrictor 

1  Black,  American  System  of  Dentistry. 


426 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


fibers.  Subjected  to  repeated  overstimulation,  they  become  inactive 
and  the  vessel  walls  yield  to  the  pressure  of  the  blood  column.  Black's 
researches  indicate  that  the  vessel  walls  may  recover  their  tone  and 
the  vasoconstrictor  nerves  their  functional  activity  after  paralysis. 
Certainly,  clinical  experience  shows  that  in  all  purely  arterial  hyper- 
emias, or  even  those  associated  with  mild  venous  hyperemia — for  the 
two  may  be  inseparable — in  cases  with  symptoms,  the  cases  can  be 
cured  if  the  causes  can  be  removed. 

Diagnosis  and  Prognosis. — Diagnosis  of  hyperemia  of  the  pulp  is 
made  through  observance  of  a  combination  of  signs  and  symptoms. 
The  symptoms  leading  to  its  detection  are  paroxysms  of  pain  induced 
by  thermal  stimuli  and  a  history  of  pain  in  the  region  in  which  this 
response  is  elicited.     The  signs  of  the  condition  in  the  order  of  their 


Fig.  356 


Dilated  bloodvessels  from  the  dental  pulp  in  hyperemia,  from  tooth  extracted  during  a 
paroxysm  of  intense  pain.      (Black.) 

importance  and  frequency  are  carious  cavities,  the  presence  of  large, 
well-made  metallic  fillings,  deep  erosions  or  abrasions,  the  presence 
of  leaking  fillings  (septic  dentine),  fractures  exposing  the  dentine, 
metallic  crowns  on  teeth  containing  vital  pulps,  sound  or  filled  teeth 
affected  by  pyorrhea,  by  infected  socket,  or  aphthous  ulcer  or  abscess 
near  by;  by  blows,  or  reflexly  from  other  teeth.  Sound  or  filled  teeth 
with  pulp  nodules,  or  hypercementosis,  may  be  diagnosticated  by  the 
a:-rays  only. 

It  is  to  be  remembered  that  arterial  hyperemia  may  be  of  several 
grades  of  severity,  according  to  the  vascular  disturl)ance. 

The  diagnosis  is  made  piin^ly  by  differentiation.  The  causes  acting 
and  other  possible  pulp  diseases  must  be  fairly  considered  and  excluded 
before  a  certain  diagnosis  can  be  made.     As  a  rule,  the  absence  of 


HYPEREMIA  OF  THE  PULP  427 

piilj)  exposure  and  the  cliaraeter  of  the  response  to  thermal  tests  are 
the  decisive  ])heiion)ena. 

The  temperature  of  the  water  used  in  testing  should  not  be  lower 
than  60°  F.,  and  should  he  applied  drop  by  drop.  A  normal  pulp  will 
rarely  respond  painfully  to  a  few  drops  of  water  at  the  temperature 
named,  flowed  into  a  cavity;  but  a  hyperemic  pulp  will  almost  invari- 
ably respond  vigorously.  As  a  rule,  a  current  of  air  from  a  chip 
blow^er  is  a  test  of  sufficient  severity. 

In  the  absence  of  a  carious  cavity  the  source  of  the  pain  is  to  be 
sought  in  large  fillings,  testing  each  tooth  by  dropping  cool  water  on 
the  filling;  in  cases  of  erosion  or  abrasion  the  test  is  made  upon  the 
exposed  dentine.  The  tooth  wdiich  responds  with  a  quick  paroxysm 
of  intense  pain,  passing  away  slowdy,  is  diagnosticated  as  the  seat  of 
pulp  hyperemia. 

In  making  this  test  doubt  may  arise  as  to  which  of  two  adjoining 
teeth  is  at  fault.  A  small  square  of  rubber  dam,  with  a  single  hole 
punched  in  its  centre,  may  be  passed  over  the  tooth  to  be  tested,  thus 
isolating  it.  As  before  stated,  however,  the  location  of  a  hyperemic 
pulp  does  not  always  mean  the  location  of  the  cause,  which  should  be 
looked  for  elsewhere  before  interfering  with  the  pulp  hyperemia. 

The  prognosis  of  arterial  hyperemia  is  favorable  for  J)ulp  conserva- 
tion in  extradental  cases  and  in  cases  of  cavities  of  decay  w^hich  admit 
of  cleansing  without  pulp  exposure,  or  in  cases  of  filled  teeth  if  the 
fillings  are  removed,  and  in  which  the  paroxysms  have  not  been  too 
severe  or  too  often  repeated.  Properly  protected  from  thermal 
shocks  the  vessels  may  recover  their  tone.  It  is  also  favorable  in 
csaes  of  light  ])l()ws  or  malocclusion  if  rest  of  the  apical  tissues  be 
secured. 

It  would  be  favorable  in  cases  of  deep  erosions  which  can  be  filled 
with  non-conductors;  but  tliis  condition  is  rarely  seen  in  erosion.  It 
is  favorable  in  fractures  without  exposure  if  caps  can  be  secured  in 
place,  but  is  unfavorable  in  ordinary  abrasions  unless  deeper  than 
the  general  occlusal  level,  or  in  sound  teeth  the  p\\]\)s  of  wiiich  are 
irritated  without  tnident  cause.  In  cases  of  actual  exposure  of  the 
pulp  it  contra-indicates  attempts  at  conservation,  except  in  the  mild- 
est varieties  and  most  favorable  circumstances,  and  then  onlv  when 
conservation  is  important.  t 

Treatment. — The  therapeutic  principles  involved  in  the  treatment 
of  this  condition  are  the  removal  of  the  source  of  irritation  and  the 
securing  of  physiological  rest.     The  treatment  is  directed   toward 


428         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

immediate  relief  of  the  existing  condition  and  the  prevention  of  its 
recurrence.  If  a  carious  cavity  exist,  it  is  to  be  freed  from  debris,  and 
the  grosser  portions  of  the  carious  dentine  are  removed;  the  pulp,  if 
unexposed,  is  to  have  the  layer  of  softened  dentine  covering  it  left 
unremoved,  if  leathery  and  not  disintegrated. 

Sedative  agents  are  imperatively  called  for;  of  those  used  the  most 
effective  being  the  oils  of  cloves  or  cinnamon,  equal  parts  of  oil  of 
cloves  and  carbolic  acid,  equal  parts  of  carbolic  acid  and  camphor 
(phenol  camphor)  a  saturated  solution  of  thymol  in  alcohol  or  of 
menthol  in  chloroform,  or  solutions  of  cocaine.  Thymol  or  menthol 
crystals  may  be  added  to  any  of  these.  These  agents  are  all  germi- 
cides as  well  as  sedatives,  and  therefore  sterilize  the  dentine  of 
cavities  in  which  they  are  sealed. 

They  are  to  be  applied  upon  a  pledget  of  cotton  and  carefully 
secured  in  place  by  means  of  temporary  stopping,  oxysulphate  of  zinc, 
soft  zinc  phospha  te,  or  facing  amalgam ;  sometimes  by  the  use  of  cotton 
and  thickened  tincture  of  benzoin  or  similar  varnish.  In  from  twenty- 
four  to  forty-eight  hours  the  tooth  is  placed  under  the  rubber  -dam 
and  excavated,  if  not  a  case  of  filling  removal ;  its  walls  are  varnished, 
and  over  the  wall  nearest  the  pulp  a  disk  of  softened  gutta-percha  is 
laid.  Over  this  zinc  phosphate  paste  is  flowed.  "Formagen"  or 
"Jodo-Formagen"  may  be  used  in  place  of  the  gutta-percha.  A  stiif 
mixture  of  eugenol  and  Hubbuck's  zinc  oxide  is  a  very  valuable  sed- 
ative cement  which  may  remain  a  time  as  a  test  and  then  be  in  part 
left  as  a  permanent  floor  covering.  It  is  usual  to  complete  such  fillings 
with  zinc  phosphate  or  gutta-percha,  to  remain  for  six  months  or 
a  year.  The  conductivity  of  zinc  phosphate  is  too  high  to  be  used 
as  the  sole  material  over  pulps  which  have  been  the  seat  of  pro- 
nounced hyperemia.  In  mild  cases  the  filling  may  be  completed  at 
once. 

If  the  pulp  be  exposed,  it  is  probably  the  part  of  wisdom  to  remove 
it  immediately  by  cocaine  anesthesia  or  by  arsenic  after  sedation; 
though  if  for  any  special  reason  capping  be  demanded,  it  may  be  done. 

If  desired,  the  protective  pocket-like  coverings  made  for  arsenical 
applications  may  be  utilized  for  the  reception  of  the  sedative  applica- 
tion.    (See  Coverings  for  Arsesnic.) 

It  not  infrequently  happens  that  it  becomes  necessary  to  assist  the 
pulp  arteries  to  recover  their  tone  by  means  of  counterirritants 
applied  to  the  gum  over  the  apex  of  the  root.  This  is  especially  true 
in  cases  of  pulp  capping.     Dental  tincture  of  iodine  (iodine,  '^'nj; 


HYPEREMIA  OF  THE  PULP  429 

alcohol,  §j;  dissolve  by  succussion;*  or  potassium  iodide,  sat.  sol., 
and  zinc  sulphate,  sat.  sol.,  aa,  with  iodine  crystals  to  complete 
saturation^)  is  to  he  applied  in  spots  to  the  gums,  or  a  mixture 
of  equal  parts  of  tincture  of  iodine  and  tincture  of  aconite  may 
be  painted  upon  the  gum.  A  mixture  made  of  two  parts  of 
tincture  of  aconite  and  one  part  of  chloroform  is  recommended  by 
Jack,^  to  be  applied  to  the  cleansed  and  dried  mucous  membrane  by 
means  of  a  pad  of  cottonoid,  one-half  inch  wide  by  three-quarters  of 
an  inch  long.  It  should  l)e  held  in  place  l)y  the  finger  for  fifteen 
seconds.  Tincture  of  aconite  upon  cotton,  placed  in  the  rul)l)er  cup 
applicator  of  a  cataphoric  apparatus  and  held  against  the  gum  for  a 
half  minute,  while  the  current  of  a  few  cells.are  active,  will  produce 
a  circumscribed  area  of  irritation  which  may  later  lose  its  epidermis. 
This  amount  of  irritation  is  valuable.  A  capsicum  plaster  may  be 
used.  For  any  case  of  obdurate  pain  systemic  sedation  or  derivation 
may  be  employed.     (See  Pulpitis.) 

In  cases  of  abrasion  or  erosion  carbolic  acid  is  applied;  an  excava- 
tion having  a  retentive  form  is  made,  which  is  varnished  and  filled; 
or  in  abrasion  the  pulp  may  require  removal.  A  tooth  containing  a 
large  metallic  filling  must  have  the  filling  removed,  and  after  reducing 
the  hyperemia  a  non-conducting  layer  must  be  placed  between  the 
pulp  and  the  filling.  The  precaution  should  always  be  taken,  when 
the  pulps  of  teeth  in  which  cavities  have  been  prepared  respond 
unduly  to  the  tenij)erature  test,  to  cover  the  dentinal  walls  with  a 
layer  of  non-conducting  material.  In  the  absence  of  this  precaution 
the  constant  overstimulation  of  the  pulp  by  thermal  impulses  con- 
ducted through  the  metallic  filling  may  at  any  time  result  in  hyper- 
emia. If  mild  hyperemia  occur  after  filling  with  metal,  it  ordinarily 
passes  away  after  a  few  weeks.  The  fibrilUe  at  first  rebel,  then 
become  tolerant,  owing  to  tubular  calcification,  etc. 

In  the  cases  due  to  apical  irritation  not  only  must  counterirritants 
be  applied  to  the  gum,  but  it  may  be  necessary  to  cap  an  adjacent 
tooth  with  a  rul)l)er  dam  guard  in  order  to  guard  against  the  irritation 
of  the  apical  tissue  by  overocclusion.     (See  Acute  Aj)i(al  Abscess.) 

If  the  hyperemia  is  of  a  gradual  onset  and  due  to  an  overoccluding 
filling  or  crown,  this  is,  of  course,  to  be  reduced  to  normal  occlusion. 
If  due  to  the  overocclusion  induced  l)y  ciironic  pyorrhea,  the  over- 
occluding  tooth  is  to  be  shortened.  If  of  acute  onset,  a  guard  may 
also  be  necessary.     As  illustrating  its  effectiveness  in  combination 

'  FlaffK.  ^  Nmthrop.  '  American  Tcxt-bnok  of  Operative  Dentistry. 


430  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

with  removal  of  the  cause,  may  be  cited  a  case  of  an  upper  third  molar 
with  a  small  pyorrhea  pocket  on  the  mesiolingual  aspect  of  the  root. 
It  overoccluded  one-thirty-second  of  an  inch,  each  bite  producing 
excruciating  local  pain,  with  also  reflex  to  the  ear.  In  twenty-four 
hours'  use  of  the  guard,  the  pocket  having  been  treated,  the  occlusion 
was  almost  normal,  the  reflex  pain  gone,  and  the  guard  was  removed 
and  the  tooth  brought  to  normal  occlusion.  In  all  cases  of  cause 
external  to  the  tooth  the  cause  alone  is  to  be  treated.  Trichloracetic 
acid,  or  silver  nitrate  in  saturated  aqueous  solution,  may  be  applied 
to  inflamed  bone  or  aphthae;  while  "dry  socket"  or  exposed  and 
ulcerated  alveolus  surface  must  be  treated  as  indicated.  (See  Index.) 
The  patient  is  to  be  directed  to  avoid  the  use  of  very  cold  or  hot 
substances. 

Idiopathic  hyperemia  occasionally  affects  teeth  in  which  there  is 
no  loss  of  enamel  or  dentine;  and  when  this  condition  occurs  it 
leads  to  suspicion  that  the  pulp  is  the  seat  of  nodular  deposits; 
though  cases  have  occurred,  particularly  of  lower  incisors,  in  which 
none  were  found  after  devitalization.  Some  form  of  apical  trauma- 
tism may  also  be  looked  for,  or  reflexes.  If  not  found,  the  pulp 
usually  requires  devitalization,  though  counterirritants  may  be  tried. 

The  test  of  success  of  remedial  measures  is  the  gradual  reduction 
of  response  to  slight  variations  in  temperature — i.  e.,  the  pulp  gradu- 
ally bears  higher  and  lower  temperatures  until,  approximately,  a 
normal  tolerance  is  established. 

As  shown  by  Jack,  this  varies  for  hot  applications  from  152°  F.  to 
118°  F.,  and  for  cold  ones  from  74°  F.  to  32°  F. 

In  order  to  determine  the  rate  of  tolerance  normal  to  the  individual, 
he  suggests  that  sound  lower  incisors  be  isolated  by  the  rubber  dam 
and  tested  by  throwing  upon  them  first  water  at  a  temperature  of 
80°  F.  The  temperature  of  the  water  is  then  gradually  lowered  or 
raised  until  slight  pain  is  produced  by  the  test.  The  point  registered 
by  the  thermometer  will  be  the  normal  limit  of  thermal  tolerance  for 
the  particular  test. 

I'he  data  gained  are  useful  in  determining  the  progress  of  a  case 
of  hyperemia. 

A  lack  of  success  in  tlic  reduction  of  the  arterial  liyj>cremia  is 
evidence  that  the  more  severe  condition  of  venous  hyperemia  has 
supervened. 

In  the  devitalization  of  hyperemic  pulps  there  is  often  painful 
reaction  to  any  of  the  means  employed.     Sedatives  should  precede 


HYPEREMIA  OF  THE  PULP  431 

arsenical  applications,  ancl  if  at  any  time  arsenic  profliice  a  painful 
hyperemia  or  aggravate  one  previously  existing,  it  must  be  removed 
anfl  sedatives  used  before  its  renewal,  or  it  may  be  applied  at  another 
portion  of  the  tooth  while  sedatives  are  kept  against  the  pulp. 

It  is  evident  that  such  a  grade  of  vascular  excitement  as  exists  in 
cases  of  exposed  dentine  is  quite  capable  of  producing  the  constructive 
diseases  of  the  pulp  described  as  secondary  dentine  and  pulp  nodules. 
On  the  other  hand,  inflammation  of  the  pulp  has  produced  resorption 
of  the  walls  of  the  pulp  chamber. 

Pulp  Irritation  from  Electric  Action. — It  is  of  quite  common 
occurrence  that  galvanic  electricity  causes  pulp  irritation.  The  cata- 
phoric current  too  long  continued  may  induce  a  hvperirritability  of 
the  pulp  amounting  in  some  cases  to  evidence  of  hyperemia,  which 
may  subside  under  proper  treatment  or  eventuate  in  pulp  death  from 
venous  hyperemia.  The  occasional  connection  of  a  newly  placed  or 
bright  amalgam  filling  with  a  gold  filling,  bridge,  plate,  or  clasp, 
through  the  medium  of  saliva  or  food  (which  amounts  practically 
to  the  same  thing),  will,  at  times,  produce  painful  galvanic  shocks  in 
a  vital  tooth.  Dr.  Franz  Trauner^  has  reported  that  such  pain  has 
been  felt  in  devitalized  teeth.  This  is  outside  of  the  editor's  experi- 
ence, and  should  not  occur  in  totally  devitalized  teeth,  as  the  electric 
current  is  a  test  for  pulp  vitality.  The  mouth  mirror,  or  a  fork 
or  pin,  touched  to  a  new  amalgam  filling  may  also  produce  the  pain, 
but  a  nickelled  steel  instrument  usually  does  not. 

Treatment. — ^^ith  cataphoresis,  the  mischief  being  accomplished, 
the  case  must  be  treated  as  other  arterial  hyperemias. 

In  the  case  of  shocks  from  the  presence  of  the  two  metals  it  may 
be  ignored  if  slight  and  the  filling  new,  as  it  will  probably  soon  pass 
away.  A  well-set  and  brightly  polished  amalgam  filling  may  be 
tarnished  if  necessary  by  touching  it  witii  a  1  per  cent,  solution  of 
silver  nitrate;  or,  if  good  color  be  a  necessity,  the  ])ulp  of  the  tooth 
may  be  well  insulated  by  means  of  a  gutta-percha  sul)stratum,  or 
the  pulp  may  be  devitalized.  If  the  fillings  be  in  adjoining  teeth,  they 
should  be  contoured  so  as  to  touch  persistently  if  possible.  If  in  the 
same  tooth,  the  fillings  should  be  coimectcd  by  either  amalgam  or 
gold. 

Painful  shock  is  sometimes  j)n)(luce(l  by  the  animal  electricity 
discharged  from  the  operator  during  dry,  cold  weather.  It  usually 
occurs  when  the  finger  is  placed  upon  a  metal  filling,  or  the  plugger 

»  See  Dental  Cosmos,  1903. 


432         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

point  is  returned  to  a  metal  filling.  Touching  the  metal  part  of  the 
chair  before  approaching  the  patient  will  obviate  this  disagreeable 
contact. 

Venous  Hyperemia  of  the  Pulp. — Definition. — By  venous  hyper- 
emia of  the  pulp  is  meant  a  condition  of  the  pulp  in  which  the  return 
of  the  blood  in  the  pulp  to  the  heart  is  mechanically  prevented. 

Causes,  Pathology,  and  Morbid  Anatomy. — ^But  two  causes  seem 
competent  to  produce  such  a  venous  hyperemia.  These  are:  (1)  a 
preexistent  arterial  hyperemia;  (2)  thrombosis  of  vessels  at  the  apex 
of  the  pulp  canal. 

In  arterial  hyperemia  the  excess  of  blood  is  contained  in  enlarged 
capillaries  and  arterial  trunks.  The  enlarged  main  trunks  or  trunk 
at  the  apex  of  the  pulp  must  compress  the  veins,  as  the  apex  of  the 
canal  is  unyielding.  In  proportion  to  the  severity  of  the  arterial 
hyperemia,  therefore,  are  the  emergent  veins  unable  to  remove  the 
blood  collected  in  the  capillaries  and  venules,  which  gradually  enlarge 
into  varicosities  in  consequence. 

It  has  been  shown  by  Hopewell-Smith^  that  thrombosis  of  the 
small  veins  and  capillaries  throughout  the  pulp  may  result  in  rupture 
of  the  arteries,  and  hemorrhagic  extravasations  occur — either  single 
or  multiple.  These  he  terms  hemorrhagic  infarcts,  although  the 
description  given  more  accurately  denotes  a  minute  venous  hyper- 
emia.    (See  Fibroid  Degeneration  of  the  Pulp.) 

Black  has  shown  that  the  diapedesis  of  red  corpuscles,  which  is  a 
characteristic  result  of  engorgement  of  the  veins  in  venous  hyper- 
emia (see  p.  117),  occurs  in  the  pulp.  Edema,  which  usually  accom- 
panies venous  hyperemia  in  other  situations,  cannot  well  occur  in 
the  pidp  because  of  its  unyielding  surroundings  (Fig.  357). 

It  is  possible,  however,  that  fluid  may  exude  into  the  perivascular 
spaces,  compressing  the  cellular  elements.  Black  has  shown  that 
deposits  of  lymph  may  thus  occur  in  pulpitis.  The  intense  con- 
gestion and  distention  of  the  vessel  walls  permit  a  free  diapedesis  of 
red  corpuscles  into  the  pulp  tissue.  Disintegration  of  the  red  cor- 
puscles may  occur  and  the  coloring  matter  of  the  corpuscles  may 
be  fliffused  through  the  dentine,  giving  it  a  pink  discoloration  tech- 
nically known  as  "suffusion."  The  infiltrated  dentine  may  then 
become  progressively  discolored  through  the  characteristic  changes 
of  color  nested  in  connection  with  gradually  decomposing  hemoglobin 
— becoming    brown   or    Ijlue,    and   finally  l)luc   black.     Cases    have 

•  Dental  CoHUios,  1907. 


HYPEREMIA  OF  THE  PULP 


433 


occurred  of  coronal  sufFusion  in  which  the  pulp  vitality  has  persisted 
for  months.  In  some  cases  the  bulbar  portion  alone  may  be  dead. 
Partial  gangrene  and  the  general  darkening  of  the  tooth  may  be 
present  even  in  a  single-rooted  tooth  with  the  pulp  partly  alive.  In 
cases  of  suffusion  even  all  the  root  of  a  molar  may  be  suffused,  and 
pericementitis,  associated  with  such  a  hyperemia,  seems  particularly 
intractable.     The  vasomotor  paralysis  is  extreme. 

Fig.  357 


Section  of  hypereniic  pulp,  showing  aneurysmal  dilatation  of  the  vessels,  extravasations  of 
blood,  and  red  blood  disks  escaped  apparently  by  diapedesis:  a,  a,  dilated  vessels;  b,  b,  b,  ex- 
travasated  blood.  Besides  this,  red  blood  disks  are  plentifully  distributed  everywhere  in  the 
neighborhood  of  the  veins.     The  tooth  was  extracted  during  a  paroxysm  of  pain.     (Black.) 

If  a  tooth  receive  a  blow  of  sufficient  severity,  its  pulp  may  die 
without  much  evidence  of  pulp  pain.  On  the  other  hand,  if  the  blow 
be  less  severe,  it  may  give  evidence  of  an  arterial  hyperemia,  gradu- 
ally increasing  in  severity. 

In  the  former  case  it  is  prol)able  that  the  bruising  of  the  apical 
tissue  produces  a  condition  of  thrombosis  at  the  apex  which  involves 
the  pulp  by  shutting  oft"  both  its  afferent  and  efferent  ves.sels.  A 
stagnation  results,  and  death  from  lack  of  nutrition  occurs.  This  is 
also  termed  "jugulation." 
28 


434         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

In  the  latter  case  the  thrombosis  has  not  occurred,  but  an  arterial 
hyperemia  is  set  up  by  the  irritation  of  the  pulp  nerves  and  may  go 
on  to  venous  hyperemia,  or,  possibly,  it  might  produce  the  extrava- 
sations leading  to  fibroid  degeneration  of  the  pulp  (which  see). 

It  is  quite  probable  that  rapid  death  of  the  pulp  in  pulpitis  is  due  to 
the  associated  venous  hyperemia. 

Kirk^  mentioned  an  interesting  case  of  venous  hyperemia  with  in- 
tense suffusion  of  all  the  teeth  as  the  result  of  hanging. 

Symptoms. — The  symptoms  of  this  condition,  in  the  absence  of 
definite  data,  can  only  be  inferential.  When  the  paroxysms  of  pain 
are  continuous,  instead  of  temporary — that  is,  when  the  pain,  instead 
of  temporarily  subsiding,  maintains  a  constant  intensity  for  hours, 
and  does  not  respond  promptly  to  sedative  therapeusis,  and  is  accom- 
panied by  a  sense  of  fulness  rather  than  sharp  agony— a  condition 
of  serious  venous  congestion  is  inferred.  The  case  from  which  Fig. 
357  was  taken  had  been  the  seat  of  intense  paroxysmal  pain  for  some 
hours. 

Prognosis. — Perfect  recovery  from  this  condition  is  extremely 
doubtful,  so  that  if  the  pulp  be  not  intentionally  devitalized  and 
removed,  it  will  undergo  degenerative  changes.  The  fact  that  pulps 
have  remained  alive  for  years,  after  having  been  the  seat  of  marked 
congestion,  scarcely  warrants  the  attempt  to  save  so  seriously  crippled 
an  organ. 

Treatment. — The  prognosis  being  doubtful,  the  pulp  should  be 
obtunded  and  devitalized.  As  the  pulp  pain  does  not  ordinarily  yield 
to  sedatives,  it  should  be  gently  exposed  if  the  excavation  does  not 
accomplish  its  exposure.  An  antiseptic  is  to  be  applied,  and  by  means 
of  a  very  sharp  puncture  probe  the  pulp  is  to  be  delicately  punctured. 
A  free  flow  of  blood  follows,  which  relieves  the  vascular  engorgement. 
When  this  is  accomplished  the  cavity  is  to  be  syringed  out  with  warm 
water,  and  a  pellet  of  cotton  containing  a  saturated  solution  of  menthol 
in  chloroform  may  be  sealed  in  the  cavity,  or  simply  retained  by 
means  of  a  second  pellet  of  cotton  saturated  with  inspissated  tincture 
of  benzoin  or  chloropercha.  After  twenty-four  hours  an  arsenical 
application  may  be  made  for  the  purpose  of  pulp  devitalization,  or 
the  pulp  may  be  removed  by  other  means  if  tolerated.  If  desired, 
the  bulb  of  the  pulp  may  be  taken  out  under  general  anesthesia,  or, 
possibly,  under  cocaine  pressure  anesthesia. 

The  extreme  paralysis  of  the  vessel  walls  is  occasionally  shown  by 

1  Private  communication. 


INFLAMMATION  OF  THE  PULP  435 

persistent  heniorrhagc  after  dcpk-tion,  and  wliicli  iv.sLst.s  ordinary 
effort  at  limitation.  In  sonio  cases  the  intense  pain  may  continne 
as  well.  The  apj)lication  to  the  pnlp  of  a  mixture  of  powdered 
thymol  and  dried  alum,  equal  parts,  taken  up  on  a  pellet  of  cotton 
moistened  with  a  saturated  solution  of  thymol  in  alcohol,  has  proved 
useful  in  some  cases.  A  general  anodyne  may  l)e  recjuired  for  relief  of 
the  pain. 

INFLAMMATION  OF  THE  PULP   (PULPITIS). 

Definition. — Pulpitis  is  the  (jccurrence  of  the  phenomena  of  inilam- 
mation  within  the  pulp  tissue.  The  characteristic  diapedesis  of  leuko- 
cytes into  the  perivascular  tissues  must  have  occurred. 

Causes. — This  morbid  anatomy  is  usually  founcK  associated  with 
diseases  of  the  tooth  cnnvn  or  pericemental  tissue  which  admit  bacteria 
to  the  pulp.  x\t  the  same  time  it  is  quite  possible  that  a  non-septic 
irritant,  such,  for  example,  as  a  partially  absorbed  extravasation  of 
red  corpuscles  or  undue  pressure  of  a  filling  upon  a  thin  lamina  of 
healthy  dentine  overlying  the  pulp,  or  an  escharotic  applied  to  the 
pulp  may  induce  the  characteristic  pathology  of  inflammation.  (See 
Inflammation,  p.  119.) 

According  to  the  character  of  the  cause,  therefore,  inflammation  of 
the  pulp  may  be  divided  into  simple  and  infective.  It  may  be  that 
a  simple  inflammation  may  become  an  infective  one  owing  to  the 
association  of  bacteria — e.  g.,  the  pressure  of  a  foreign  body  may 
initiate  the  process  and  the  inflamed  pulp  become  a  soil  for  the  propa- 
gation of  the  bacteria  present. 

The  causes  of  pulpitis  may  be  grouj)ed  under  three  headings: 

1.  ^Mechanical  or  physical  causes,  which  irritate  by  acting  as  foreign 
bodies,  or  by  pressure. 

2.  Chemical  causes,  which  act  as  irritants  by  either  producing  a 
chemical  destruction  of  pulp  tissue,  or  by  irritation  without  direct 
destruction.  In  the  former  case  the  dead  tissue  acts  as  a  foreign  body 
against  which  the  pulp  reacts  in  an  effort  to  cause  its  exfoliation  or 
absorption. 

3.  Parasitic  or  infective,  which  cause  the  phenomena  of  infective 
inflammation. 

Pulpitis  is  classified,  according  to  its  extent,  into  partial  and  com- 
plete; according  to  its  duration,  into  acute  and  chronic;  according  to 
its  infective  character,  into  purulent  and  non-purulent;  and,  again, 


436         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

according  to  the  character  of  the  degeneration  which  follows  upon 
the  inflammatory  process.  While  pathologically  these  conditions  may 
be  clearly  differentiated  from  one  another,  they  may  be  reduced  to 
more  compact  groupings  according  to  their  clinical  significance.  For 
example,  acute  pulpitis  is  frequently  infective,  partial,  and  purulent; 
chronic  pulpitis  is  frequently  non-infective,  extensive,  non-purulent, 
and  followed  by  secondary  degenerations.  It  is,  however,  often 
purulent,  and,  of  course,  infective. 

For  the  sake  of  convenienGC,  pulpitis  will  receive  a  clinical  division 
into  acute  and  chronic. 

Acute  Pulpitis. — By  acute  pulpitis  is  meant  that  form  of  inflam- 
mation of  the  pulp  which  runs  an  active  and  more  or  less  violent  course 
toward  pulp  death,  and  has  associated  with  it  acute  paroxysms  of  pain. 

Causes. — ^The  causes   of   acute  pulpitis  are    direct    and    indirect, 
intrinsic  and  extrinsic;    the  vast  majority  of   cases  being  due  to 
extrinsic  causes.    The   direct  intrinsic  causes  are  hemorrhagic  ex- 
travasations accompanying  venous  congestion,  or  thrombosis,  pulp 
nodules,  and  injury  of  the  vessels  at  the  apex  of  the  root.    The  direct 
extrinsic  causes   are,   perhaps,   invariably  associated  with  bacterial 
invasion,  a  possible  exception  being  the  pressure  of  filling  material 
upon  a  thin  elastic  lamina  of  softened  dentine,  covering  the  pulp.    The 
dental  pulp  is  intolerant  of  the  slightest  pressure,  and  rebels  vigorously 
when  subjected  to  compression.     Irritating  drugs  may  also  act  as 
irritants — e.  g.,  zinc  chloride.    It  is  not  necessary^  that  the  pulp  should 
be  exposed  to  permit  bacterial  infection,  and  direct  or  extensive  bac- 
terial invasion  is  probably  not  necessary  for  the  production  of  pulpitis. 
The  waste  products,  ptomains,  etc. ,  of  bacteria  may  find  their  way  to 
the  surface  of  the  pulp  via  the  dentinal  tubuli,  through  a  layer  of  soft- 
ened dentine,  and  excite  inflammation.    It  is  extremely  probable  that 
infection  of  the  pulp  is  an  invariable  consequence  of  its  exposure;  but 
as  a  pulp  may  be  exposed  without  subjective  evidences  of  hyperemia  or 
inflammation,   it  follows  that  infection  does  not  necessarily  imply 
inflammation,  though  the  absence  of  acute  symptoms  may  be  ac- 
counted for  by  the  escape  of  the  effusions  into  the  cavity  of  decay. 
The  presence  of  a  gross  irritant,  such  as  a  mass  of  food  debris, 
vegetable  seeds,  bread-crumbs,  etc.,  in  contact  with  the  pulp  will 
precipitate  an  acute  inflammation  in  which  bacterial  relations  must 
be  taken  into  consideration. 

"The  severity  of  the  inflammation  does  not  appear  to  be  proportion- 

1  Miller,  Dental  Cosmos,  1894. 


INFLAMMATION  OF  THE  PULP  437 

ate  to  the  number  of  bacteria  present,  and  in  a  highly  inflamed  pulp  we 
may  be  able  to  find  hut  few  bacteria.  .  .  .  The  conclusion  seems 
to  be  justified  that  the  inflammation  is  due  to  the  combined  action 
of  the  bacteria  and  their  products  (acids,  ptomains,  etc.)  with  which 
the  carious  dentine  becomes  impregnated."^  Goadby  has,  however, 
shown  that  the  Streptococcus  brevis  and  Bacillus  necrodentalis  may 
pass  through  the  tubules  of  even  secondary  dentine. 

Pulpitis  from  injury  of  the  vessels  at  the  apex  of  the  pulp  must  be 
mentioned.  It  may  occur  in  consequence  of  blows,  biting  upon  hard 
substances,  too  rapid  wedging,  the  rapid  movement  of  teeth  in  ortho- 
dontia, and  the  progressive  loosening  of  teeth  in  pyorrhea  alveolaris. 

Fig.  358 


Inflammation  of  dental  pup:  a,  a,  normal  cells;  b,  b,  b,  b,  inflammatory  elements;  c,  cells  in 
process  of  division  (^q  inch).     (Black.) 

In  these  cases  the  pericementum  is  also  affected  and  the  teeth  are 
tender  upon  percussion.  Pain  in  the  teeth  upon  assuming  the  recum- 
bent position,  dull,  heavy  uneasiness  about  the  jaws,  and  inordinate 
response  to  thermal  stimuli,  particularly  to  heat,  point  to  pulpitis. 
Bacteria  from  an  abscess  on  an  adjoining  tooth,  from  a  pyorrhea 
pocket,  or  the  pressure  of  an  impacted  tooth  may  also  act  as  causes. 

Morbid  Anatomy  and  Pathology. — In  determining  the  existence  of 
pulpitis,  no  matter  what  the  symptoms  which  have  presented  or  the 
condition  as  to  expo.sure,  etc.,  the  microscopic  examination  of  sections 
of  the  affected  organ  constitutes  the  only  decisive  test;  if  the  changes 
characteristic  of  inflammation  be.  absent,  no  matter  what  the  symp- 
toms, pulpitis  did  not  exist.  The  essential  feature  of  the  process  is 
emigration  of  the  white  blood  corpuscles  from  the  small  veins  into  the 
intercellular  matrix  of  the  pulp.     At  first  the  inflammatory  elements 

'  Miller,  Dental  Cosmos,  1S94. 


438 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


(leukccvtes)  are  scattered  through  the  spaces  between  the  pulp  cells 
(Fig.  35S);  at  a  later  stage  the  territory  is  ccciipied  by  round  indiffer- 


FiG.  359 


Interstitial  pulpitis  with  pulp  nodule  in  situ.      (V.  A.  Latham.) 

ent  cells  alone.     The  inflammation  may  be  widespread,  as  shown  in 
Fig.  359,  or  may  be  localized  to  some  portion  of  the  pulp,  as  one  horn 


Minute  inflammatory  focus  within  the  tissues  of  the  pulp:  a,  a,  arterial  twigs;  h,  a  nerve  bundle; 
c,  collection  of  leukocytes.     (Black.) 

of  a  pulp;  Black  noted  also  inflammatory  action  occurring  in  small 
i.slands  (Fig.  300). 

Swelling  of  the  pulp — exudation— cannot  occur    unless  there  be  a 


INFLAMMATION  OF  THE  PULP  439 

break  in  the  wall  of  the  j)iilj)  cliaiiiher  thr()U<;h  which  additional  space 
can  he  gained.  Black  has  recorded  that  "he  found  beneath  the  layer 
of  odontoblasts  in  the  region  of  an  exposure  an  unmistakable  deposit 
of  inflanniiatorv  lymph.  The  case  had  a  history  of  severe  toothache 
for  two  days,  two  weeks  previously.  The  pulp  exhibited  evidences  of 
previous  extravasations  of  blood  from  hyperemia." 

There  is  evidence  that  the  pidp  may  recover  from  attacks  of  inflam- 
mation, and  that  resolution  occurs.  In  some  cases,  as  shown  under  the 
head  of  calcareous  degeneration,  the  tissues  may  become  infiltrated 
with  calcic  material.  In  others,  chronic  degenerative  changes — 
inflammatory  degeneration — may  supervene. 

The  cases  thus  far  described  have  been  given  as  non-infective, 
simply  because  their  infective  character  has  not  been  clearly  made 
out,  although  it  is  very  probable  that  they  are  infective. 

Suppuration  of  the  pulp  is  a  common  accompaniment  of  pulp  inflam- 
mation; this,  being  necessarily  infective,  will  be  described  separately. 

GaskelP  has  reported  a  case  where  a  central  incisoi-  entirely  free 
from  caries  exhibited  on  its  palatal  aspect  a  pinkish  tinge,  which 
increased  in  depth  until  the  enamel  overlying  crushed  in,  revealing 
the  pulp  of  the  tooth  lying  immediately  beneath;  there  had  been  a 
resorption  of  a  large  mass  of  the  dentine  lying  between  the  pulp  and 
the  enamel.  The  pidp  was  removed  and  the  tooth  filled.  Xo  history 
is  given  as  to  the  condition  of  the  root,  whether  resorption  had  occurred 
there  or  not.  Shortly  after,  the  adjoining  central  incisor  exhibited 
a  like  pink  coloration,  which  increased,  leading  to  the  inference  that 
resorption  was  in  progress  in  this  tooth  also.  At  the  suggestion  of 
E.  C.  Kirk  the  patient  received  continued  doses  of  arsenic  iodide  and 
the  compound  syrup  of  the  hypophosphites,  in  the  hope  of  inducing 
a  general  and  local  constructive  metani()rj)hosis.  This  treatment  was 
followed  by  a  gradual  disappearance  of  the  j)ink  coloration,  an  evi- 
dence of  a  redeposition  of  dentine.  In  the  absence  of  histological  data 
it  is  impossible  to  state  just  what  was  the  nature  of  the  rej)air  tissue  in 
this  particular  ca.se,  but  Miller^  has  shown  that  the  j^dp  may  take  up 
a  resorptive  function  and  remove  dentine  which  inav  later  be  re(fej)os- 
ited  as  anomalous  tissue.  The  new  dentine  does  not  contain  tubules, 
but  has  the  characteristics  of  cemental  tissue"^  (osteodentine),  or  even 
bone  with  Haversian  systems^  (Fig.  3G1).     This  process  has  its  ana- 

'  Proceedings  of  tlie  Academy  of  Stomatology,  Pliilailel|ihia,  1895. 
'Dental  Cosmos,  August,  1901. 

^  Hopewell-Smitli,  Histology  and  Patliohistology  of  the  Teeth. 
«  Salter. 


440 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


logue  in  the  tusks  of  elephants  and  also  in  the  production  of  Howship's 
lacunae  in  the  resorption  of  the  cementum  by  the  pericementum,  these 
lacunae  later  being  filled  up  with  cementum. 

Symptoms. — The  early  stage  of  inflammation  is  an  arterial  hyper- 
emia, and  as  the  leukocytes  collect  in  the  venules  a  venous  hyperemia 
is  established.  No  matter  how  far  the  area  of  stasis  extends,  beyond 
it  will  exist  an  area  of  arterial  hyperemia.  Owing  to  the  enclosing 
canal  walls  and  constricted  apex  a  general  venous  hyperemia  may  be 
established  which  causes  the  death  of  the  pulp. 

In  view  of  these  facts  it  is  not  surprising  that  the  symptoms  of  pulp 
inflammation  take  on  somewhat  the  characteristics  of  both  arterial 


Fig.  361 


Resorption  of  the  walls  of  the  pulp  chainber  and  redeposition  of  new  calcific  matter:  a,  pulp 
chamber;  6,  c,  d,  portions  of  resorption  areas  not  refilled  and  walled  off  by  the  new  deposit- 
forming  cavities  occupied  originally  by  the  pulp  tissue.     (Miller.) 


and  venous  hyperemia.  The  diapedesis  of  leukocytes  and  exudation 
of  fluid  cause  the  phenomena  of  heavy  boring  pain  and  a  feeling  of 
internal  pressure. 

The  pulp  may  be  exposed  and  no  symptoms  be  present.  A  sudden 
pressure  of  food  or  toothpick,  suction  upon  the  pulp  or  the  contact  of 
cold  or  hot,  salt,  sweet,  or  acid  sul)stances  may  excite  an  attack  of  throb- 
bing or  lancinating  pain.  This  may  be  localized  in  the  tooth  or  may 
be  reflected  to  other  teeth  or  the  parts  mentioned  under  hyperemia. 

The  assumption  of  the  recumbent  position  permits  an  increased 
flow  of  l)lo(jd  into  the  paretic  vessels  of  the  pulp  and  increased  suffer- 


INFLAMMATION  OF  THE  PULP  441 

ing  results  in  correspondence  witli  the  law  that  inflamed  parts  are 
always  more  painful  in  the  dependent  position.  (See  Pathological 
First  Dentition.)  Indeed,  recumbency  is  sufficient  at  times  to  induce  a 
paroxysm  in  a  comparatively  quiet  but  inflamed  pulp.  Under  a 
capping  or  filling  pressing  on  the  pulp  or  thin  dentine  the  pain  may 
begin  as  a  slight  pain  and  gradually  increase  in  intensity,  or  it  may 
respond  as  a  sudden  agony,  beginning  even  some  time  after  the  oper- 
ation. In  the  later  stage  of  pulp  inflammation  the  pain  is  of  a  heavy, 
boring,  continuous  character,  the  pericementum  becomes  somewhat 
hyperemic,  and  the  tooth  responds  to  tapping.  In  case  of  a  highly 
irritable  pulp,  however,  the  concussion  of  the  pulp  produced  by 
tapping  may  readily  cause  pain. 

In  pulpitis  the  pulp  responds  both  to  heat  and  cold,  but,  as  a  rule, 
more  to  the  former  than  to  the  latter. 

Diagnosis. — ^The  diagnosis  is  largely  inferential  and  made  by  obser- 
vation of  the  symptoms  and  conditions  existing.  The  pulp  may  be 
exposed  or  closely  approached  by  caries,  or  the  pulp  may  be  approx- 
imated by  a  large  filling.  If  there  be  a  leak  about  the  filling,  a  septic 
fluid  or  actual  decay  beneath  the  filling  may  be  the  exciting  cause. 
In  the  absence  of  evident  causes  such  sepsis  is  always  to  have  con- 
sideration, and,  if  necessary,  the  filling  must  be  removed  and  tests 
applied.  The  more  obscure  causes,  such  as  abscesses  upon  adjoining 
teeth,  infection  from  the  pericemental  tract  in  the  course  of  pyorrhea, 
looseness  of  teeth  or  traumatisms,  are  to  be  carefully  considered.  If 
the  tooth  involved  be  uncertain,  each  tooth  should  be  placed  under 
rubber  dam  and  tested  thoroughly. 

Prognosis. — The  prognosis  is  always  bad  for  the  comfortable  conser- 
vation of  the  pulp,  and  it  should  be  removed  and  the  canal  filled. 

Treatment. — The  treatment  of  pulpitis  involves  the  reduction  of  the 
amount  of  blood  in  the  vessels  of  the  pulj),  the  sterilization  of  the 
infected  area,  the  relief  from  the  pain,  and  the  removal  of  the 
pulp.  It  is  usual  to  excavate  the  cavity  of  decay  thoroughly 
enough  to  remove  from  over  the  pulp  decayed  dentine  which 
would  prevent  the  action  of  remedies  or  act  as  an  irritant.  The 
cavity  is  then  washed  and  one  of  the  essential  oils  or  phenol 
camphor,  with  or  without  menthol,  thymol,  or  cocaine  added, 
saturated  solutions  of  cocaine  in  glycerin.  1")  per  cent,  chloral 
hydrate  in  glycerin,  "cocaine-phenate"  (sat.  sol.  cocaine  in  carbolic 
acid),  "thymophen"^  (carbolic  acid  crystals  and   thymol  crystals  aa 

«Kirk. 


442  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

to  a  liquid),  thvmol  in  alcohol,  or  menthol  in  chloroform  or  carbolic 
acid,  or  a  mixture  of  acetate  of  morphine  with  oil  of  cloves  or  creosote 
is  placed  in  it  on  cotton.  The  addition  of  a  trifle  of  powdered  alum 
to  any  of  the  above  sedatives  acts  as  an  astringent  to  the  vessels. 
During  the  half  hour  succeeding  the  application  the  pulp  should  give 
some  indication  of  relief.  If  it  be  somewhat  decided,  a  portion  of  the 
remedy  used  should,  if  possible,  be  sealed  in  the  cavity  for  twenty- 
four  hours.  The  covering  may  be  prepared  first  as  for  arsenic.  (See 
Coverings  for  Arsenic.)  If  not  possible  to  seal  it  in,  it  may  be  covered 
with  cotton  saturated  with  a  varnish  made  by  evaporating  tincture  of 
benzoin.  This  varnish  hardens  like  sandarac  varnish,  but,  unlike  it, 
is  not  irritant. 

If,  after  the  first  half  hour,  no  indication  of  relief  has  been  obtained, 
it  is  well  to  expose  the  pulp  and  to  relieve  the  engorged  vessels  by 
delicately  puncturing  it.  (See  Extirpation  of  Pulp.)  After  exposing 
the  pulp  it  will  perhaps  exude  a  bead  of  pus,  which  makes  the  diag- 
nosis one  of  pulp  suppuration.  After  free  bleeding,  which  may  be 
encouraged  by  means  of  warm  water,  the  sedatives  will  usually  act. 
It  may  be  necessary  at  times  to  employ  general  anesthesia  (nitrous 
oxide  gas)  as  a  means  to  obtain  free  bloodletting.  Everything  being 
prepared,  the  patient  is  anesthetized  and  the  bulb  of  the  pulp  cut 
out,  or  in  a  single-rooted  tooth  the  entire  pulp  may  be  taken  out.  At 
times  cocaine  pressure  anesthesia  is  effective  at  least  for  the  removal 
of  the  bulb  of  the  inflamed  pulp,  and  sometimes  of  the  entire  pulp. 

In  case  of  partial  extirpation,  not  only  is  free  bleeding  induced,  but 
the  diseased  pulp  tissue  is  largely  removed.  When  hemorrhage  ceases 
arsenic  may  be  applied.  If  the  hemorrhage  be  obstinate  the  applica- 
tion of  powdered  thymol  and  dried  alum  may  be  used.  (  See  Venous 
Hyperemia.)  When  sedatives  are  used  upon  the  pulp,  counterirritants 
applied  to  the  gum  are  aids  of  great  value,  and  are  to  be  used  as 
described  under  Arterial  Hyperemia.     (See  p.  428.) 

Instead  of  these  the  principle  of  depletion  may  be  employed.  Deep 
cuts  may  be  made  with  a  sharp  l)istoury  in  the  gum  overlying  the 
root  apex.  The  anastomosis  with  the  vessels  of  the  apical  tissue  is 
expected  to  cause  the  cuts  to  act  as  openings  made  in  veins  leading 
from  the  inflamed  pulp.  According  to  Nancrede,  depletion  on  the 
venous  side  of  an  inflamed  area  markedly  reduces  engorgement.  In 
addition  to  these  measures  catharsis  is  a  valuable  means  of  derivation; 
a  tablespoonful  of  sulphate  of  magnesia  is  to  be  dissolved  in  a  goblet 
of  water  and  taken  internally  at  least  a  half  hour  before  a  meal. 


SUPPURATIOX  OF  THE  PULP  443 

If  the  ])ain  he  ohdiii-alc  and  its  rctiii'ii  Tcan-d,  two  !,-(;raiii  .siilj>liate 
of  morphine  tablets  niav  he  disiK-iised,  j)refeial»ly  hy  the  operator, 
to  he  taken  only  in  case  of  severe  })ain  and  an  hour  apart.  Acetanilide 
and  phenaoetin  are  also  useful. 

The  following  is  a  u.seful  anodyne  and  antineural<,nc  j)re.scription : 

I^. — Phenacetin, 

Acetanilide aa     gr.  xxx 

Quinia  sulph gr.  xv. — M. 

Divide  into  six  capsules. 
S. — One  morning  and  evening. 
(See  also  Treatment  of  Facial  Neuralgia.) 

Quiet  of  the  pulp  must  ))e  secured  l)efore  an  arsenical  application 
is  made,  or  the  latter  merely  increases  the  irritation  instead  of  promptly 
devitalizing.  Should  such  an  irritation  occur  or  he  feared,  arsenic  may 
he  sealed  in  an  opening  made  in  another  part  of  the  tooth  (a  "  pocket"'), 
with  a  view  to  devitalizing  the  pulj)  through  an  avenue  of  healthy  ])nl|) 
tissue.  At  the  same  time  the  pnlp  may  he  (juieted  l)y  sedative  applica- 
tions made  in  the  cavity  of  decay. 

Instead  of  drilling  a  special  pit,  the  arsenic  may  he  applied  at  a 
portion  of  healthy  deutine  in  the  cavity  which  is  at  some  distance  from 
the  orifice  of  exposure;  over  the  latter  the  analgesic  may  he  placed. 


SUPPURATION  OF  THE  PULP. 

Definition. — By  suppuration  of  the  dental  pulji  is  meant  a  formation 
of  pus  on  its  surface  (ulceration)  or  in  its  sul)stance  (ahsce.ss).  It 
occurs  hoth  as  an  acute  and  as  a  chronic  att'ection. 

Causes. — The  immediate  cause  of  su])})u ration  of  the  })ul|)  is  tiie 
ingress  of  pyogenic  organisms  to  the  j)ulp.  As  in  inflammation  of  the 
pulp,  while  usually  associated  with  direct  exposure  of  the  pulp,  .suppu- 
ration may  occur  in  ])ulps  covered  hv  softened  or  even  unsoftened 
dentine. 

Arkovy^  first  observed  infection  of  the  ]>ul|)  while  still  covered  hy 
a  layer  of  unsoftened  dentine  (Fig.  3()2). 

Goadhy  has  shown  that  microorganisms  may  penetrate  even 
secondary  dentine,  a  condition  not  infre(|uently  seen  (Fig.  371). 

Miller  states  that  sections  of  the  overlying  dentine  in  a  case  of 
suppuration  of  the  pnlp  showed  the  same  forms  of  bacteria  as  were 
found  in  the  j)ulj)  itself. 

'  Flagg.  -  niagnostik  der  Zaiinkrankheiten. 


444 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


Fig.  362 


Bacteria  which  have  entered  the  body  through  wounds,  etc.,  may  be 
deposited  in  the  pulp  as  well  as  in  any  other  part  of  the  body,  wherever 
there  may  be  a  locus  minoris  resistentice  at  the  time,    ^^hile  bacteria 

may  thus  enter  from  the  circulation,  there 
is  usually  abundant  opportunity  for  their 
entrance  from  the  mouth.  Suppuration 
of  the  pulp  is  a  not  infrequent  sequel  of 
the  capping  of  pulps  which  have  given 
evidence  of  a  previous  hyperemia  or 
inflammation. 

Morbid  Anatomy  and  Pathology. — 
Anatomically  pulp  suppuration  (puru- 
lent or  pyogenic  pulpitis),  is  of  two 
general  varieties:  one  begins  upon  or 
close  to  the  surface  of  an  exposed  pulp, 
and  gradually  destroys  the  organ  through 


Invasion  of  pulp  by  micrococci. 
(Arkovy.) 


Fig.  363 


A,  diagram  of  lower  molar  with  caries  at  a  which  expo.ses  the  pulp;  the  darkened  portion  at 
b  shows  the  extent  of  the  inflammation;  the  rest  of  the  organ  was  free  from  inflammatory 
change.  B,  illustration  of  the  inflamed  tissue,  showing  a  part  destroyed  by  suppuration  at  a; 
the  odontoblasts  are  undermined  at  h;  the  Vjloodvessels  whicli  were  filled  with  blood-clot  in 
the  section  are  left  blank  here,  that  they  may  be  more  apparent.     (Black.) 

a  process  of  progressive  ulceration   (Fig.  363);  the  second,  that  con- 
fined in  the  substance  of  the  pulp,  causes  the  gradual  destruction 


SUPPURATION  OF  THE  PULP 


445 


of   a   part   of    the    pulp   through    the  formation    of   circumscribed 
abscesses  (Fig.  364). 

Ulceration  of  the  Pulp. — Of  these  two  forms,  ulceration  is  the 
more  common.     The  capillaries  (Fig.  363)  are  blocked  with  coagu- 


FiG.  364 


Acute  suppurative  pulpitis  in  the  coronal  portion;  /,  intensely  inflamed  horn;  .4,  abscess; 
V,  bloodvessels  engorged  with  blood;  S,  superficially  inflamed  horn;  .V,  nest  of  inflammation. 
X  10.     (Bodecker.) 

lated  blood  (they  are  left  open  in  the  illustration  to  clearly  mark  their 
position);  the  intercapillary  meshwork  is  occupied  by  inflammatory 
exudation;  the  surface  of  the  pulp  is  eroded  and  covered  with  pus 


446 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


corpuscles;  the  ulcerative  process  is  undermining  the  layer  of  odonto- 
blasts. The  suppurative  process  penetrates  the  body  of  the  pulp, 
following  the  direction  of  its  veins  and  hollowing  out  the  organ  into 
a  deep  cavern.  Black  regards  the  persistence  of  the  layer  of  odon- 
toblasts as  indicating  an  inferior  vitality,  as  it  shows  they  are'  less 
susceptible  of  change  of  form  than  the  other  cells  of  the  organ. 

The  process  of  ulceration  may  continue  for  weeks  or  months  until 
the  entire  organ  has  been  destroyed  molecularly.  The  necrotic  por- 
tions undergo  putrefactive  decomposition,  probably  passing  through 
the  same  stages  that  any  albuminous  substance  passes  in  its  serial 


Fig.  365 


Fig.  366 


Fig.  367 


Fig.  368 


'  .7  jf  • 


/\ ' 


J 


--> 


MiorourKanisiris  loiind  in  cultures  from  gangrenous  pulp.     (Miller.) 

(k composition,    into   tlie   end   products — ammonia,   carbon   dioxide, 
hydrogen  siilphifk-,  and  water. 

"Very  interesting  and  instructive  results  were  obtained  by  exam- 
ining material  from  different  parts  of  the  same  tooth.  In  the  case 
illustrated  in  Mg.  'M')^)  the  pulp  chamber  at  a  was  wide  open  and 
filled  with  Food  pjirliclcs,  which  had  a,  foul,  half-putrid  odor;  at  h  the 
pulp  was  putrid  and  foul-smelling;  at  c  there  was  a  small  abscess, 
filled  with  pure  white  pus,  while  the  tissue  between  this  point  and  the 
apex  of  the  root  was  highly  infiamed  and  bright  red.  Material  from 
the  pulp  chamber  (Fig.  'M\^),  a)  contained  the  forms  .shown  in  Fig. 
306;  material  from  jjoint  b  those  shown  in  Fig.  367,  and  from  the 
point  c  those  shown  in  Fig.  36S.     We  perceive  a  gradual  diminution 


SUPPURATION  OF  THE  PULP  447 

of  the  large  cocci,  and  the  appeuranee  of  small,  delicate  cocci  and 
diploeocci"  (Miller)/ 

Symptoms. — If  the  cavity  of  decay  he  open  the  pus  and  serous 
exudate  may  freely  escape,  so  that  the  symptoms  may  not  exceed  a 
dull,  gnawing  pain,  which  is  usually  reflex  in  character. 

As  a  ride,  the  response  to  cold  will  be  much  delayed  or  even  absent. 
Intense  pain  may  exist  when  the  pus  cannot  find  exit  owing  to  food 
debris  being  massed  in  the  pulp  chamber,  or  owing  to  the  presence 
of  a  filling  or  mass  of  secondary  dentine.  The  case  then  resembles, 
and  practically  becomes,  one  of  abscess  of  the  pulp. 

The  chief  diagnostic  feature  of  pulp  ulceration  is  the  presence  of 
the  subacute  inflammatory  symptoms  described  above  and  the  pres- 
ence of  a  pulp  partially  removed  by  decomposition  of  its  upper  portion. 

Thus,  if  the  pulp  chamber  be  open  at  one  horn,  and  a  probe  may 
be  passed  into  it  for  a  short  distance  until  it  comes  into  contact  with 
an  irritable  portion  of  {)ulp,  and  when  withdrawn  have  the  odor  of 
putrefaction,  the  diagnosis  is  clear — loss  of  pulp  substance  by  putre- 
factive changes,  presumably  by  suppuration.  In  some  teeth  it  may 
be  by  partial  gangrene.  Many  phases  of  this  condition  may  be  seen; 
thus,  in  an  extreme  case  one  canal  of  a  lower  molar  contained  a  highly 
irritable  vital  filament  of  pnlp  extending  but  one-quarter  inch  from 
the  apical  foramen;  a  second  canal  was  entirely  occupied  by  a  per- 
fectly vital  but  ulcerating  filament;  the  third  canal  contained  an 
entirely  dead  pulp.  The  bulb  of  the  pulp  had  disappeared,  doubt- 
less by  suppuration. 

Treatment. — The  treatment  of  pulp  idceration  in  its  early  stages 
involves  the  opening  of  the  orifice  of  exposure,  the  sterilization  of 
the  superficies  of  the  pulp,  and  pulp  removal. 

Superficial  sterilization  may  be  accomplished  by  removing  the  pus 
or  putrefactive  material  present  by  means  of  warm  3  per  cent,  hydro- 
gen dioxide  or  a  50  per  cent,  solution  of  meditrina.  The  saturated 
solutions  of  thymol  in  alcohol  or  menthol  in  chloroform,  or  2  per 
cent,  formaldehyde,  may  be  sealed  in  position  against  the  pulp  for 
twenty-four  hours  as  a  sedative  antiseptic.  The  application  of 
arsenic  may  (hen  be  safely  made. 

In  fav()rabl(>  cases  the  l)uli)  of  (he  pulj),  or  even  (he  en(ire  pulp, 
may  be  removed  at  the  first  or  second  sitting  by  means  of  cautiously 
applied  cocaine  pressure  anesthesia.  In  somcvcases,  however,  the 
patient  will  rebel. 

'  Dental  Cosmos,  1894. 


448         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

When  a  part  of  the  canal  filaments  alone  remain,  after  syringing 
to  remove  pus,  the  pressure  anesthesia  may  be  resorted  to.  A  long 
thread  of  cotton  is  saturated  with  carbolic  acid  or  carbolic  acid 
and  cocaine,  and  gently  packed  into  the  canal  against  the  pulp 
filament.  Pressure  with  vulcanizable  rubber  is  now  produced, 
and  after  a  few  minutes  the  pulp  will  be  sterilized  and  anesthe- 
tized sufficiently  for  removal.  Puncturing  is  also  useful  at  times 
(which  see).  Arsenic  may  be  cautiously  placed  on  cotton  half  way 
up  a  canal  against  such  a  pulp  filament.  Another  method  consists  of 
packing  a  thread  of  cotton  dipped  in  carbolic  acid  tightly  against  the 
filament,  in  which  thrombosis  is  thus  induced. 

Abscess  of  the  Pulp. — Abscess  of  the  pulp  is  usually  situated  near 
the  point  of  exposure  of  the  organ.  It  may  be  confined  to  one  horn 
of  the  pulp,  or  may  involve  nearly  the  entire  substance  of  the  pulp, 
the  peripheral  tissue  of  the  pulp  being  unbroken.  Abscess  may  exist 
at  some  distance  beneath  the  surface  of  the  pulp,  and  the  latter  be 
still  covered  with  a  layer  of  dentine.  Burchard  once  uncovered  the 
horn  of  a  molar  pulp  which  was  covered  by  a  lamina  of  hard  dentine, 
and  no  fluid  appeared;  but  upon  passing  a  sharp  probe  into  the  white 
area  of  exposure  for  over  one-eighth  of  an  inch  or  more  there  was  a 
free  flow  of  pus  which  quickly  filled  the  larger  carious  cavity.  A  pulp 
removed  entire  from  a  tooth,  and  which  was  yellowish  white  in  color 
and  unbroken,  showed  upon  section  its  interior  hollowed  out  into  an 
enormous  abscess  cavity  (Fig.  370).  The  bloodvessels  were  blocked; 
the  peripheral  tissues  were  unaltered;  between  the  odontoblasts  and 
the  abscess  cavity,  the  latter  lined  the  pus  corpuscles,  evidences  of 
inflammation  were  plenty.  Black  found  that  the  odontoblasts 
retained  their  form  after  neighboring  cells  of  the  pulp  had  been 
destroyed. 

Miller's^  researches  show  a  preponderance  of  cocci  and  micrococci 
in  cases  of  enclosed  abscess;  cocci  and  diplococci  were  of  constant 
occurrence.  Many  of  the  forms,  both  cocci  and  bacilli,  were  cultivable 
upon  gelatin  and  agar-agar.  Some  of  them,  cocci  and  bacilli,  brought 
about  the  liquofaction  of  gelatin;  others  did  not.  So  that  it  must  be 
inferred  that  infective  inflammation  and  necrosis  of  the  pulp  may 
occur  without  suppuration.  (See  Gangrene  of  the  Pulp.)  In  some 
instances  streptococci  were  found.  In  the  freely  exposed  pulps 
varieties  of  organisms  were  found  which  would  render  clear  the 
possibility  of  a  general  infection  by  way  of  the  dental  pulp, 

•  Dental  Coamoa,  1894. 


SUPPURATION  OF  THE  PULP 


449 


Symptoms. — The  usual  symptoms  aie  as  follows:  In  a  tooth  con- 
tainiuo;  an  enormous  filling,  one  in  which  the  pulp  has  been  exposed, 
or  in  a  tooth  having  a  large  carious  cavity,  the  patient  gives  a  history 
of  discomfort  or  decided  pain,  appearing  at  intervals,  sometimes 
appearing  and  disappearing  suddenly,  the  existing  condition  having 
been  ushered  in  by  dull,  gnawing  pain,  which  is  usually  not  positively 
located,  although  it  may  be.  The  pain  grows  in  intensity,  and,  in 
contradistinction  to  the  pulp  conditions  previously  described,  pain  is 
relieved  instead  of  increased  by  applications  of  cold.  It  may  be, 
however,  that  the  prolonged  contact  of  ice-water  may  induce  a  response. 
The  response  to  heat  is  marked,  so  that  a  mouthful  of  hot  coffee  or 


Fig.  370 


Transverse  section  of  inferior  bicuspid  i)ulp,  one-half  diagrammatic:  a,  abscess  cavity;  h,  em- 
bryonic cells  at  tlie  peripliery  of  tiie  abscess  cavity;  c,  occluded  bloodvessels.       (Burchard.) 

even  the  warmth  of  the  tongue  may  precipitate  an  attack  of  severe 
and  continued  pain.  Pain  produced  upon  passing  from  a  warm  to 
a  cold  atmosphere,  and  vice  versa,  is  also  symptomatic.  If  the  pulp 
be  freely  exposed  and  pricked  with  a  sharp  instrument,  a  flow  of  pus 
follows  in  many  cases,  and  the  relief  is  almost  immediate.  In  the 
earlier  stages  a  period  of  throbbing  pain  may  follow  evacuation  of 
the  pus. 

In  other  cases  the  response  to  heat  may  decrease  until  it  is  almost 
absent,  and  the  case  only  be  seen  when  evidences  of  the  action  of 
bacterial  products  upon  the  pericementum  appear,  which  they  usually 
do  in  the  later  stages  of  pulp  suppuration,  when  the  tooth  becomes 
loose,  extruded,  and  tender  upon  percussion. 
29 


450 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


Fig.  371 


The  symptoms  of  pericemental  disturbance  may  simulate  those  of 
incipient,  acute,  apical  abscess,  even  though  a  quarter  of  an  inch  or 
more  of  apical  pulp  tissue  exist  in  a  vital  though  highly  inflamed 
condition.  Upon  clinical  evidence  it  is  assumed  that  the  inflammation 
of  the  pulp  produces  inflammation  of  the  apical  tissue  (Fig.  371). 
In  one  case  the  gum  and  contiguous  parts  about  an  upper  molar  were 
swollen,  apical  abscess  diagnosticated,  and  a  free  flow  of  pus  fol- 
lowed by  blood  obtained  upon  opening  the  crown.  An  examination 
made  twenty-four  hours  later,  after  symptoms  had  subsided,  demon- 
strated all  three  pulp  filaments  to  be  alive  when  a  post  hoc  diagnosis 
of  extensive  abscess  of  the  pulp  was  made.  If  untreated,  symptoms 
of  pulp  and  pericemental  disturbance  may  disappear  for  weeks  or 

months;  but  if  the  parts  be  not  per- 
fectly sterilized  and  reinfection  pre- 
vented, it  is  only  a  question  of  time 
when  septic  pericementitis  will  arise. 
Diagnosis. — The  most  valuable  diag- 
nostic sign  is  the  peculiar  reaction  to 
thermal  stimuli — the  decreasing,  then 
absent  response  to  cold,  and  the  in- 
creasing reaction  to  applications  of 
heat.  This  reaction,  together  with 
the  continued  gnawing  and  full  sen- 
sation in  the  tooth,  usually  affords  a 
diagnosis  which  is  confirmed  by  evacu- 
ating pus  from  the  pulp,  which  exudes 
usually  as  a  minute  bead  followed  by 
blood,  although  the  reverse  order  may  obtain. 

In  cases  where  several  teeth  are  involved  in  the  diagnosis,  differ- 
entiation is  made  by  isolation  of  each  tooth  by  means  of  a  small  square 
of  rubber  dam.  The  thermal  test  is  then  applied.  The  presence  of 
a  quantity  of  secondary  dentine  will  confuse  by  causing  dulness  of 
response.  In  such  case  the  electric  test  should  be  resorted  to.  (See 
Dry  Gangrene.)  In  some  cases  secondary  dentine  will  have  formed 
in  the  pulp  cavity  and  the  abscess  may  be  found  in  one  of  the  filaments, 
while  the  other  will  be  apparently  healthy.  Fig.  371  is  a  diagram  of 
a  number  of  cases  seen  in  practice. 

Prognosis. — General  experience  regards  ulceration  and  abscess 
of  (he  |)iilp  as  precursors  of  the  death  of  the  organ.  Usually  this  is 
by  })n)gn'ssiv('  siip|)iiratioii.      It  is  iiiidonbtedly  true,  however,  that 


Abscess  of  the  pulp  after  formation 
of  a  large  amount  of  secondary  den- 
tine, dividing  the  pulp  into  two  por- 
tions: S  D,  secondary  dentine;  V  P, 
vital  pulp;  A  P,  abscess  or  confined 
pus;  /,  area  of  apical  inflammation. 
(Diagrammatic.)  (After  case  in  the 
mouth.) 


SUPPURATION  OF  THE  PULP 


451 


attempts  at  circumvallatioii  of  the  dead  tissue  aiv  made  in  some 
cases  (Fig.  372).  The  pus  cells  under<ro  (le<,aneration  and  the 
abscess  site  may  be  the  seat  of  calcareous  deposits,     \i\xn\  in  these 


KiG.  372 


Chronic  supiiurative  jMilpitis  tcriniiiatiiiijc  in  calfificatioti  of  tlie  |)ii>  and  atro|>hy  of  tlic  |)ul|>: 
A^,  larger  abscess,  filled  with  oalcificd  pus;  .1-,  abscess  at  the  periphery  of  the  pulp;  .1',  .4', 
small  lonnitudiiuil  abscesses,  all  calcified;  N,  calcified  nerve  bundle;  C,  C.  calcareous  deposi- 
tions in  the  fibrous  pulp  tissue;  /-",  /',  pigment  clusters  from  previous  hemorrhage.  X  10. 
(Bodecker.) 

cases  death    is  delayed,   not   averted.     The   remainder  of   the   pulp 
undtM-yoes  atroj)liic  chani>;es,  and  commonly  suppuration  reapjuars. 

Treatment. — The  treatment  of  the  ca.se  consists   in   relievin<j:  the 
existing  pain,  completing  the  devitalization  of  the  pulp,  and  rt  moving 


452         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

it  in  such  a  manner  that  no  organisms  or  dead  matter  are  carried, 
beyond  the  apex  of  the  root. 

To  secure  relief,  evacuation  of  the  pus  is  imperatively  necessary. 
The  organ  is  freely  exposed,  exercising  no  pressure  in  gaining  free 
access  to  it.  If  pus  do  not  flow  upon  exposure  of  the  surface  of  the 
pulp,  a  sharp,  slender,  sterilized  probe  is  quickly  passed  into  the 
substance  of  the  pulp,  when,  if  pus  be  present,  it  will  usually  escape 
freely  through  the  opening  thus  made  and  be  followed  by  blood. 

If  the  pus  formation  be  limited  and  circumscribed,  throbbing  pain 
may  follow,  which  promptly  quiets  under  an  application  of  cocaine  in 
glycerin.  The  application  is  not  made  until  the  pus  flow  ceases.  A 
pellet  of  cotton  wet  with  a  1  per  cent,  solution  of  formalin,  or  a  satu- 
rated solution  of  thymol  in  alcohol  or  other  antiseptic  sedative,  is 
laid  upon  the  pulp  and  the  cavity  is  sealed  for  twenty-four  hours 
(never  longer),  and  then  an  arsenical  application  is  made.  Should 
the  exposed  portion  of  the  pulp  be  insensitive  it  is  cut  away  until 
access  is  had  to  the  vital  portion,  where  the  arsenic  is  to  be  applied. 
The  pulp  may  sometimes  be  anesthetized  by  cocaine  for  removal. 
In  these  cases  it  is  necessary  to  place  cocaine  in  the  canal  on  cotton 
and  produce  direct  pressure  on  each  canal  filament.  General  cavity 
pressure  will  probably  fail.  The  rubber  dam  need  not  necessarily 
be  applied  for  the  treatment  preliminary  to  devitalization,  but  the 
pulp  should  be  kept  under  the  influence  of  antiseptics. 


CHRONIC  INFLAMMATION  OF  THE  PULP. 

In  cases  in  which  the  resistive  force  of  the  pulp  is  great  and  the 
causes  of  less  violent  nature  or  less  violent  in  action,  the  inflammation 
may  Ik'  of  low  grade  anrl  continue  for  some  time.  Pulp  ulceration 
may  pursue  a  chronic  course,  as  has  already  l)een  described.  Abscess 
of  the  pulp  may  also  become  chronic,  and  the  pulp  may  even  encapsule 
the  pus  area,  and,  the  bacteria  dying,  the  abscess  area  may  become 
the  seat  of  calcareous  deposits. 

Sclerosis  of  the  Pulp. — Inflammation  of  a  low  grade  may  persist 
in  the  pulp  for  long  periods,  giving  rise  to  an  increase  of  its  fibrous 
tissue  with  atrophy  of  the  cellular  elements,  producing  a  condition 
found  in  chronic  interstitial  inflammation  in  some  other  tissues — a 
sclerosis.  Instead  of  the  usual  (Iistri})ution  of  myxomatous  tissue, 
bands   and    bundles   of   fibrous   tissue   appear.     The   pulp   appears 


CHRONIC  INFLAMMATION  OF  THE  PULP 


453 


shrunken  and  stiff,  bloodvessels  are  contrartcd  and  sclerotic,  and  the 
nerve  fibers  have  undergone  partial  or  complete  atrophy  and  degen- 
eration (Figs.  373  and  374). 

Fig.  373 


h 


^'01  J., 

9  IKr'e  o  .  •^yJSmwS 


^  :  ».»._,■       ,,     - '  -    •  . 
Chronic  inflammation  of  the  pulp,  areolation,  and  degeneration.     (Black.) 

Black  found  that  in  the  late  stages  of  sclerotic  atrophy  areolae 
developed  in  the  bundles  of  connective  tissue,  the  inflammatorv 
elements  having  disappeared  and  the  areolae  being  occupied  by  fluid. 

Fig.  374 


Pulpitis  arteriosclerosis;  nerve  degeneration.      (V.  .A.  Latham.) 

Arkovy  describes   the  condition  as   reticular  atrophv  of   the   pulp 
(Fig.  373). 
The  condition  would  point,  as  suggested  by  Black,  to  venous  hyper- 


454 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


emia  as  the  cause  of  the  edema  rather  than  inflammation;  but  the 
evidences  of  former  chronic  inflammation  in  the  existence  of  the 
bundles  of  reticulated  tissue  show  this  to  have  been  the  essential  con- 
dition. The  observations  of  the  same  writer  indicate  that  atrophy 
of  the  odontoblasts  is  a  usual  accompaniment  of  all  of  the  chronic 
pulp  affections. 

Sclerotic   and   other  chronic   degenerations   of   the   pulp  usually 
present  the  history  of  one  or  more  attacks  of  pulpitis  in  the  past,  with 

Fig.  375 


A,  a  first  lower  molar  with  a  cavity  at  a  completely  filled  by  an  hypertrophy  of  the  pulp, 
which  lias  grown  out  througli  the  orifice,  exposing  the  pulp  at  b.  B,  a  field  illustrating  the 
tissue  of  the  growtli,  which  is  composed  almost  entirely  of  granulation  tissue  of  a  very  primi- 
tive type:  n,  a  covering  of  epithelium  presenting  papilla?;  b,  epithelium  apparently  without 
papilla;.     (Black.) 

more  or  less  continuous  uneasiness  extending  over  a  long  period. 
The  response  of  the  pulp  to  all  tests  becomes  diminished  and  dull. 

Treatment. — Such  pul])s  are  to  be  devitalized  and  removed. 

Chronic  Hyperplastic  (Hypertrophic)  Pulpitis. — \Vh(>n  the  pulp 
is  exposed  over  a  wide  area,  long-continued  chronic  inflammation 
may  lead  to  an  enlargement  of  the  organ  with  a  protrusion  of  an 
altered  pulp  mass  through  the  orifice  of  exposure,  producing  the 
condition  known  clinically  as  fungous  pulp.  When  the  growth 
extends  beyond  the  boundaries  of  the  orifice  and  then  increases  in 


CHRONIC  INFLAMMATION  OF  THE  PULP 


455 


bulk  it  forms  a  petkinculated  mass  to  wliicli  the  torin  j)olypus  of  the 
pulp  has  been  applied. 

Morbid  Anatomy  and  Pathology.— The  growth  has  its  origin  in  a 
chronic  inflammation  of  the  body  of  the  ])ulp;  the  organ  swells,  and 
contact  with  the  sharp  edges  of  the  orifice  of  exposure  excites  a  con- 
tinued irritation,  leading  to  further  proliferation  of  the  cells  of  the 

Fig.  376 


M. 


Hyperplastic  myxomatous  pulp,  which  filled  a  carious  cavity:  M ,  lobules  made  up  of  papillse 
of  a  myxomatous  .structure,  rich  in  caiiillary  and  venous  bloodvessels;  G,  calcareous  globule; 
E,  epithelial  cover  of  jiapilhe.      X  10.     (Bodecker.') 

inflamed  part,  so  that  a  large  mass  of  embryonic  ti.s.sue  is  formed 
(Fig.  375),  termed  by  Black  granulation  tissue  of  a  low  type.  As  in 
the  granulation  tis.sue  of  repair,  bloodvessels  grow  into  this  mass, 
so  that  it  may  bleed  at  a  slight  touch.  Black  noted  in  his  case 
illustrated  a  covering  of  squamous  epithelium  upon  the  periphery 
of  the  growth,  which  might  be  interpreted  as  the  transformation  of 


456 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


mesoblastic  into  epiblastic  tissue,  but  the  correct  explanation  beyond 
doubt  is  that  advanced  by  the  same  author,  that  the  epithelium  is 
transplanted  from  the  gums,  and  grows  after  the  manner  of  a  skin 
graft.     The  growth  does  not  contain  nerves. 

These  grow^ths  may  undergo  further  changes;  higher  organization 
of  the  granulation  tissue  occurs  and  fibrous  tissue  is  formed ;  the  cells 
may  undergo  degenerations,  first  granular,  then  fatty,  and  suppu- 
ration and  gangrene  may  occur.  Tomes^  records  a  case  where 
calcification  of  an  hypertrophied  section  of  a  pulp  occurred;  but  as 


Fig.  377 


Acute  pulpitis:  .S,  secondary  dentine;  B,  bay-like  excavations  filled  with  medullary  or  inflam- 
matory corpuscles;  V,  transverse  section  of  a  bloodvessel;  M,  multinuclear  body.  X  300. 
(Bodecker.)- 

the  case  was  due  to  traumatism  (fracture  of  a  tooth),  different  vital 
conditions  existed  from  those  in  the  cases  under  discussion.  Actual 
calcification  of  the  mass  is  scarcely  possible,  although  calcareous 
degeneration  may  occur  within  the  fungous  mass  (Fig.  376). 

Resorption  of  the  walls  of  the  pulp  chainl)er  may  occur  as  an 
accompaniment  of  chronic  pulpitis.  What  appears  to  l)e  an  idio- 
pathic dentine  resorption  is  described  on  p.  439.  Black  records  a 
case  where,  after  pulp  capping  in  a  lower  molar  and  the  insertion 
of  a  large  gold  filling,  the  tooth  was  examined  at  the  end  of  ten  years; 

*  Dental  Surgery,  third  edition. 


CHRONIC  INFLAMMATION  OF  THE  PULP 


457 


for  two  or  three  years  the  pulp  had  given  evidences  of  irritability, 
and  when  the  pulp  was  removed  the  pulj)  ehainher  was  found  enor- 
mously enlarged  and  opening  into  the  pericementum  between  the 
roots  of  the  teeth.  Fig.  377  exhibits  resorption  of  previously  formed 
secondary  dentine  with  the  probable  agency  through  which  the 
resorption  is  brought  about.  The  area  of  resorption  is  invaded  by 
numerous  multinucleated  cells,  which  are  evidently  performing  the 
function  of  odontoclasts. 


Fig.  378 


Fig.  379 


Fig.  380 


Fig.  381 


Hypertrophy  of  pulps.     (Garretsou.) 

As  shown  by  Miller,  Hopewell-Smith,  and  others,  a  reconstructive 
change  may  occur  and  adventitious  dentine  be  redeposited  in  the 
area  of  resorption  (Fig.  301). 

Symptoms. — The  symptoms  of  chronic  pulp  inflammations  and 
degenerations  are  usually  those  of  long-continued  discomfort,  with 
reflex  pains,  which  rarely  persist  into  the  latest  stages  of  degeneration. 
The  response  to  heat  and  cold,  present  at  first,  declines  until  the  pulp 
scarcely  reacts,  and  then  but  slowly. 


Fig.  382 


Fig.  383 


Hypertrophy  of  the  gum.     (Garretson.)         Hypertrophy  of  the  pericementum.     (Garretson.) 

No  nerve  fibers  develop  in  the  hypertrophic  pulp  tis.sue,  so  that  the 
newgrowth  has  no  sensitivity  in  it.self,  although  pressure  upon  it 
may  cause  sharp  pain  through  the  still  vital  pulp  nerves  themselves. 

Four  or  five  of  the.se  hy})ertrophies  may  exist  in  a  mouth,  filling 
whole  cavities  of  decay,  the  surrounding  tooth  structure  being  in 
various  stages  of  disintegration.  They  seem  to  be  comparatively 
insensitive  to  mastication  (Fig,  379). 

Hypertrophy  of  the  pulp  also  may  be  a.ssociated  with  pulp  ulcera- 
tion, the  growth  arising  from  one  canal  of  a  tooth. 


458  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

Regeneration  of  an  extirpated  pulp  has  been  claimed,  but  I  have 
never  seen  any  cases  that  were  not  referable  to  the  above  form  of 
hvpertrophy,  or  to  a  fungoid  growth  from  the  pericementum. 

Diagnosis. — The  only  condition  with  which  hypertrophic  pulp  may 
be  confounded  is  a  pedunculated  growth  of  gum  tissue  through  a 
cavity  at  the  neck  of  a  tooth  beneath  the  gum  margin  or  through  a 
perforation  either  accidental  or  by  caries  (Fig.  383).  It  is  impor- 
tant to  differentiate  between  these  conditions,  because,  if  an  appli- 
cation of  arsenical  paste  be  made  to  a  fungous  gum,  the  destruction 
of  tissue  may  extend  into  the  sound  pericementum.  The  physical 
appearances  of  the  two  are  alike:  they  both  bleed  freely  and  have 
about  the  same  degree  of  sensitivity. 

Histological  examination  of  this  class  of  hypertrophy  of  the  gums, 
conducted  by  Dr.  Luigi  Ancone,^  of  Italy,  demonstrated  that  the 
growth  is  a  simple  exaggeration  of  the  normal  elements  of  the  part. 

If  the  tumor  be  central  to  the  tooth  tissue  and  the  latter  not  decayed 
out  to  very  thin  walls,  it  may  be  at  times  laid  aside  by  means  of  a 
blunt  instrument  and  be  seen  to  have  its  origin  from  an  orifice  of 
exposure  (Fig.  378).  As  a  rule,  a  hyperplastic  pericementum  will 
be  found  to  have  its  attachment  much  lower  or  more  lateral  than 
a  hyperplastic  pulp,  and  the  pulp  cavity  be  seen  to  have  been 
enlarged  by  caries,  even  more  than  shown  in  Fig.  315.  It  is  then 
fairly  inferred  to  be  a  pulp  mass,  especially  if  the  tooth  has  never 
been  operated  upon.  The  diagnosis  may  be  a  doubtful  one,  in 
which  case  the  rubber  dam  is  to  be  applied,  the  polypus  frozen  by 
means  of  a  spray  of  ethyl  or  methyl  chloride,  and  the  mass  removed 
with  a  sharp  blade  passed  across  its  peduncle. 

The  source  of  the  tumor  may  then  be  usually  clearly  seen.  As  an 
alternative  proceeding  the  tissue  may  be  thoroughly  saturated  with  a 
strong  solution  of  trichloracetic  acid  and  then  ablated.  If  any  further 
doubt  exist,  the  pulp  is  to  be  sterilized  with  hydrogen  dioxide,  etc., 
and  a  pellet  of  cotton  saturated  with  oil  of  cloves,  carbolic  acid,  or 
dental  tincture  of  iodine  is  laid  upon  it,  and  over  this  temporary 
stopping  is  firmly  packed.  By  this  means  the  growth  may  be  pressed 
away  until  it  is  seen  to  arise  from  either  a  pulp  chamber  or  a  perfora- 
tion made  by  decay  or  accidental  excavation  into  the  pericemental 
tract. 

Pressure  anesthesia  may  be  resorted  to  partly  as  a  diagnostic 
measure.     In  such  case  no  danger  exists  beyond  the  possible  forcing 

'  Abstract  from  I'Odontologia,  by  Dr.  W.  Dunn,  in  International  Uental  Journal,  1899. 


CIIROXIC  IXFLAMMATinX  OF   rilK  PULP 


459 


of  cocaine  into  the  \f\\\w  tissue.  Xcrvocidin  should  be  useful  in 
cases  of  doubt.  Skiagraphy  should  afford  a  diat^nosis.  Hemorrhage 
may  be  checked  with  alum  and  thymol  in  powder  or  solution. 

Treatment. — If  the  ease  be  one  of  pulj)  hypertrophy,  arsenic  may 
be  applied  or  pressure  anesthesia  attenij)ted  for  J)ulp  removal. 

Crystals  of  iodine  have  been  used  with  satisfaction  in  combination 
with  pressure  for  pnlp  devitalization.^     If  a  perforation  exist,  it  is  to 

Fig.  384 


//,  liemorrliaKic  infarct;  /?,  rupture  of  bloodvessel;  D,  dentine;  O,  vacuolated  odontoblasts; 
F,  early  fibrosis  of  pulp.       X   250.      (Hopewell-Smidi.) 

be  treated  by  sealing  the  orifice  with  gutta-))ereha  or  copper  amal- 
gam, if  practicable.      (See  Therapeutics  of  Dental  Caries.) 

Infarction  of  the  Pulp. — The  pn duction  of  infarction  may  result 
as  described  under  Fibroid  Degeneration,  and  consist  of  minute 
circumscribed  hemorrhages  from  end  arteries  into  the  pulp  tissue 
(Fig.  384). 

'  Truman. 


460 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


Fibroid  Degeneration  of  the  Pulp. — ^Apart  from  the  degenerations 
due  to  inflammatory  conditions,  a  form  of  degeneration  occurs  "as  a 


Fig.  385 


DO 


DO 


Horizontal  section  of  fibroid  degeneration  of  the  pulp  in  aitu.  Prepared  by  Mr.  Hopewell- 
Smith's  process:  D,  deeply  stained  dentine;  S,  large  areolar  spaces;  D  O,  degenerate  odonto- 
blasts; P,  fibroid  tissue  of  pulp.      X  45.     (Hopewell-Smith.) 

natural  old-age  termination  of  the  life  of  a  healthy  pulp,"  and  similar 
to  senile  changes  occurring  in  the  pericementum.  (See  Fibroid 
Degeneration    of   Pericementum.)     This   change,   as    described    by 


DEGENERATION  OF  THE  PULP 


461 


Hopewell-Smith/  occurs  in  teeth  of  the  aged  in  whose  mouths 
simple  alveolar  resorption  has  occurred,  though  later  hc^  has  shown 
that  it  may  occur  in  the  pulps  lof  young  persons,  in  sound  teeth 
extracted  for  irregularity,  and  even  in  teeth  in  which  the  dentinal 
wall  or  pulp  cavity  is  not  completed  to  a  typical  calcification.  He 
regards  it  as  due  to  a  primary  thrombosis  of  the  capillaries  and  veins, 
with  permanent  dilatation  of  the  arteries,  with  or  without  tiny  hem- 
orrhages (infarcts),  the  lack  of  collateral  circulation  and  lymphatics 


Fig.  386 


—  FO 


Fibroid  degeneration  of  the  pulp:     D,  dentine  with  tubules;   V  O,  fibroid  odontoblasts; 
I',  atrophied  pulp  tissue. 


contributing  to  the  atrophy.  As  a  cause  he  suggests  chemical 
changes  in  the  blood  through  systemic  derangement,  as  anemia, 
chlorosis,  or  exhaustive  diseases,  the  red  corpuscles  being  fewer  and 
the  leukocytes  and  blood  platelets  increased,  thus  favoring  a  throm- 
bosis of  small  ves.sels;  also,  that  here  inflammatory  changes  in  the 
pericemental  tissue  might  interfere  with  the  pulp  circulation  suffi- 
ciently to  produce  it. 


Histology  and  Pathohistology  of  the  Teeth. 


'  Dental  Cosmos,  1907. 


Fig.  387 


Fatty  degeneration  of  the  pulp.      (V    A.  Lathana.) 
Fig.  388 


.'•^     A 


y-  'i/''- 


/<  ..>> 


r" 


^•■^ 


•A  J 


Cloudy  hwelliiin;  .pareiicliyiiiat(ju.i  deKenerali(jn;    pulp  iioiluhjM.      (V.  A.  Latham.) 


DEGENERATION  OF  THE  PULP 


463 


Clinical  Significance. — While  the  form  of  thrombosis  or  filirosis 
may  not  he  (hai^nosticated  because  of  hiek  of  related  symptoms. 
Hopewell-Smith  ar<ijues  that  they  should  be  suspected  in  weak  and 
unhealthy  j)atients,  and  that  such  suspicion  should  contra-indicate 
conservative  operations,  also  that  they  may  explain  certain  difficulties 
of  devitalization  or  anesthetization  of  the  pulp  or  cause  a  related 
change  in  the  pericementum  or  brittleness  in  the  dentine. 

Morbid  Anatomy. — The  odontoblasts  become  sheaved  with  or 
without  fatty  degeneration;  the  arteries,  permanently  tlistenderl, 
undergo  hyaline  degeneration;  a  reticular  atrophy  occurs,  with  dis- 

FiG.  389 


Colloid  iloKeiieration  of  the  pulp.      Comi).are  with  Fig.  49.      (V.  A    Latham.) 

appearance  of  cells  and  nuclei  of  both  pulj)  and  vessels  and  nerves, 
and,  at  the  .same  time,  the  connective-tissue  hbers  undergo  hyjK>rplasia. 
I'he  pulp  goes  more  or  less  gradually  through  the  stages  shown  in 
Fig.  384,  finally  producing  the  stage  shown  in  Figs.  385  and  386,  in 
which  the  pulps  are  shrunken  and  may  have  left  the  wall  of  the  pulp 
chamber.  Many  areolar  spaces  appear  which  may  be  arranged  in 
chains.  The  odontoblasts  are  degenerated.  The  pulp  stroma  is 
very  (lens(>,  has  a  clear,  fibrous  structun>,  becomes  very  marked  in 
staining,  and  is  highly  differentiated  from  the  surrounding  tis.sue. 
The  bloodvessels,  nerves,  cells,  and  connective  tissue  have  all  dis- 
appeared, and  their  place  is  taken  by  a  new,  firm,  fibrous  structure 


464  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

devoid  of  cells,  nuclei,  or  any  regular  arrangement  of  constituent 
parts. 

''There  is  no  calcification  of  the  pulp  and  no  obliteration  of  the 
dentinal  tubules. 

"  The  proximate  cause  and  associate  phenomena  are  not  as  yet 
clearly  related." 

Fatty  Degeneration  of  the  Pulp. — During  the  course  of  degenera- 
tion of  the  elements  of  the  pulp  fatty  changes  may  occur  as  in  other 

Fig.  390 


A 


X 


Great  thickening  of  nerve  bundle.      From  a  case  of  chronic  neuralgia       Patient  had 
many  teeth  extracted  for  neiiriti'^.      (V.  A.  Latham.) 

parts.     The  fatty  changes  occur  in  the  walls  of  the  arteries  and 

sheaths  of  the  nerves,  and  in  the  odontoblasts.^ 

Cloudy  swelling  also  appears.     (Latham.)      (See  p.  75.) 

Colloid  Degeneration  of  the  pulp. — The  demonstration  of  colloid 

material  within  the  pulp  has  been  made  by  Latham,  as  shown  in  Fig. 

389.     She  states  that  it  may  become  calcified.    The  condition  is  very 

rare. 
Nerve-end    Degeneration   of   the   Pulp.— The  degeneration  of 

nerves  occurs  in  the  ]>ulp  as  it  may  in  the  pericementum  and  from 

the  same  causes  that  produce  endarteritis.      The  bundles  may  be 

enlarged.     Neuralgia  may  be  associated  with  it. 

•  Hopewell-Smith. 


DEGENERATION  OF  THE  PULP 


465 


Neoplasm  of  the  Pulp. — Latham  claims  that  iieo{)lasm  may 
occur  ill  the  pulp,  and  offers  the  photomicrograph  shown  in  Fig.  391 
as  proof  of  the  fact. 

Many  of  the  destructive  pulp  diseases  occur  in  the  pulps  of  the 
temporary  teeth,  and  are  to  be  treated  in  like  manner,  except  as  to 
the   use   of  arsenic,  which,   being   accompanied  l)y  greater  danger, 

Fig.  391 


Neoplasm  of  the  pulp.      (V.  A.  Latham.) 

should,  for  the  most  part,  be  replaced  by  nervoeidin,  pressure  anes- 
thesia, or  cantharides.  This  point  is  discussed  at  length  in  the  chapter 
upon  Removal  of  the  Pulp. 

If  the  tooth  roots  be  largely  resorbed,  the  pulp  may  bear  capping 
with  a  paste  composed  of  oxide  of  zinc  and  eugenol,  even  when  ulcer- 
ation has  occurred.  The  pulj)  may  die  under  this  capping,  when  the 
case  is  further  treated  as  indicated.     (See  Chronic  Apical  Abscess.) 


30 


CHAPTER    XVI  I. 

METHODS   OF  REMOVAL  OF  THE   DENTAL  PULP  AND 
ROOT-CANAL  FILLING. 

The  removal  of  the  dental  pulp  being  a  valued,  and  in  some  cases 
the  only,  method  of  curing  certain  pulp  diseases,  a  consideration  of 
the  methods  available  is  of  importance. 

1.  Under  the  influence  of  a  general  anesthetic,  nitrous  oxide  or 
even  ether,  the  pulp  cavity  may  be  opened  and  the  pulp  removed. 
The  influence  of  nitrous  oxide,  as  ordinarily  administered,  will  be  too 
evanescent  to  permit  removal  of  root  filaments  of  pulps  of  multi- 
rooted teeth.  In  these,  therefore,  the  removal  of  the  pulp  bulb  alone 
is,  as  a  rule,  accomplished.  By  this  means  the  pulp  is  depleted 
and  the  engorgement  of  the  pulp  vessels  reduced.  The  devitalization 
is  completed  with  arsenic,  or  by  cocaine  pressure  or  nervocidin 
anesthesia. 

In  single-rooted  teeth  the  pulp  chamber  may  be  opened  with  a 
sharp  bur  and  the  pulp  quickly  removed  with  a  barbed  broach. 
Under  the  influence  of  ether  the  operation  may  be  made  complete  in 
any  tooth.     It  is  seldom  used  for  the  purpose. 

2.  Sprays  of  rapidly  vaporizable  substances,  such  as  ethyl  or 
methyl  chloride,  directed  against  the  exposed  pulp,  the  tooth  being 
isolated  under  rubber  dam,  will,  in  some  cases,  render  the  pulp 
entirely  insensitive,  although,  as  a  rule,  they  fail  to  entirely  anes- 
thetize to  the  apical  foramen.  The  method  is  painful  and  not 
applicable  in  many  cases  of  highly  irritable  pulps. 

3.  Applications  of  even  saturated  solutions  of  cocaine  being  inef- 
fective, it  has  been  suggested  to  inject  cocaine  into  the  pulp:  the 
surface  of  the  pulp  is  benumbed  by  applications  of  strong  solutions 
of  cocaine,  the  needle  of  a  hypodermic  syringe  containing  a  solution 
of  cocaine  hydrochlorate  (from  4  per  cent,  to  10  per  cent.)  is  thrust 
mto  the  pulp  canal,  and  a  drop  of  the  solution  forcibly  injected;  in  a 
few  seconds  the  pulp  may  be  so  benumbed  that  it  can  })e  removed.^ 

'  Maxfield,  Proceedings  of  the  New  Jersey  State  Dental  Society,  1.894. 


REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING     467 

This  procedure,  however,  appears  to  fail  as  often  as  it  succeeds.  A 
strong  sokition  of  silver  nitrate  has  been  suggested  by  Dr.  A.  N. 
Gaylord  as  useful  in  place  of  the  cocaine  before  applying  the  needle. 
The  injection  of  cocaine  into  the  gum  over  the  apex  of  the  root  for 
nerve-trunk  anesthesia  may  at  times  be  employed,  though  only  indi- 
cated in  case  simpler  methods,  to  be  described,  are  not  feasible. 
(See  Hypersensitive  Dentine.) 

4.  Cocaine  cataphoresis  is  usually  effective,  although  in  conditions 
of  active  hyperemia  and  inflammation  even  the  maximum  current 
and  saturated  solutions  of  the  alkaloid  may  fail  to  subdue  the  irrita- 
bility of  the  pulp.  In  favorable  cases  about  fifteen  minutes  are 
required  for  pulp  anesthesia,  a  10  or  15  per  cent,  solution  being 
employed. 

5.  A  more  reliable  method  of  utilizing  cocaine  is  in  combination 
with  pressure.  The  rubber  dam  is  applied.  A  small  pellet  of  amadou 
(spunk)  is  wet  with  a  saturated  solution  of  cocaine  hydrochlorate  in 
water,  alcohol,  or  chloroform,  and  laid  upon  the  pulp  and  a  strip 
of  soft,  unvulcanized  rubber  is  folded  into  the  cavity  until  it  fills  it. 
A  burnisher  as  large  as  convenient  is  then  used  to  gently  press  the 
rubber  in  the  direction  of  the  pulp.  A  piece  of  amadou  placed  over 
the  rubber  will  concentrate  the  force  of  the  burnisher  and  prevent 
egress  of  the  rubber.  A  slight  pain  will  be  produced,  upon  indication 
of  which  further  pressure  should  cease  for  the  time,  but  the  advance 
made  be  maintained.  In  a  half  minute  pressure  may  be  again 
renewed,  and,  unless  pain  be  produced,  be  increased  until  the  full 
force  of  the  wrist  is  exerted,  though  less  pressure  is  sufficient.  The 
rubber  and  spunk  are  then  removed,  the  pulp  cavity  opened,  and  the 
pulp  lifted  away  with  a  broach.  For  multi-rooted  teeth  a  more 
prolonged  pressure  is  required  than  for  the  single-rooted.  On 
account  of  possible  non-removal,  or  difficult  removal,  of  some  portion 
of  ptdp  tissue  in  fine  roots,  it  may  be  well  to  instil  carl)olic  acid  into 
the  fine  canals  to  prevent  return  of  sensation.  By  this  operation  the 
pulp  tissue  is  visibly  compressed,  and  in  some  cases  ischemia  with  its 
accompanying  lessening  of  sensibility  is  produced;  at  the  same  time 
the  cocaine  is  probably  forced  into  the  pulp  tissue  and  even  into  the 
apical  tissue.  In  some  cases  the  anesthesia  is  satisfactory,  while  the 
pulp  itself  still  bleeds  readily,  so  that  cocaine  anesthesia  seems  the 
most  satisfactory  explanation.  The  o{)eration  appears  to  fail  in  the 
teeth  M'ith  very  large  foramina,  though  with  the  moderately  large 
foramina  it  is,  as  a  rule,  successful.     Some  pulps  rebel  totally  against 


468    REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

the  treatment.  In  a  few  cases  both  attempt  at  pressure  and  release 
of  pressure  have  been  equally  painful,  and  without  anesthesia.  In 
some  cases  each  increase  of  pressure  has  been  felt,  but  the  anesthesia 
has  nevertheless  occurred.  In  case  of  an  open  canal  the  ^^Jlcanite 
is  to  be  carefully  packed  into  it  in  a  small  quantity,  not  overflowing 
into  the  general  cavity,  and  the  pressure  is  to  be  accurately  made. 
Some  pulps  require  several  applications,  and  some  are  not  affected  at 
all  by  the  second  application.  The  application  sometimes  stops  acute 
pain  and  sometimes  produces  it  in  a  fairly  quiet  pulp.  In  all  these 
the  conditions  may  seem  favorable  to  the  attempt.  The  effect  seems 
most  pronounced  when  the  exposure  is  free  and  the  pressure  effected 
in  a  direct  line  with  the  pulp  axis.  For  this  reason  a  second  appli- 
cation may  be  successful,  while  the  first  may  only  permit  a  better 
exposure.  The  dentine  may  be  anesthetized  by  the  method  in  order 
to  gain  an  exposure  in  cases  of  sound  teeth  from  which  it  is  desired 
to  remove  pulps  by  this  method.  In  some  cases  it  is  necessary  to 
close  the  buccal  and  lingual  interdental  openings  by  means  of  the 
thumb  and  forefinger  in  order  to  concentrate  the  force  exerted  upon 
the  pulp.  The  force  should  be  carefully  applied  in  cases  of  frail  walls. 
These  are  perhaps  better  cut  away.  In  some  cases,  where  all  walls 
are  broken  away,  it  may  be  necessary  to  use  the  tip  of  a  finger.  In 
cases  of  ulcerated  pulp  filaments  the  above-described  pressure  may  be 
modified.  A  thread  of  cotton  may  be  saturated  with  carbolic  acid,  or 
carbolic  acid  and  cocaine,  and  packed  into  contact  with  the  pulp  and 
the  pressure  with  vulcanite  rubber  made.  Some  caution  should  be 
observed  in  the  use  of  both  cataphoresis  and  pressure  anesthesia 
after  partial  devitalization  by  the  use  of  arsenic,  as  cases  have  been 
recorded  of  the  carriage  of  the  latter  to  the  apical  tissues  by  these 
means.  The  obvious  indication  is  the  thorough  removal  of  all 
arsenic  and  dead  tissue  before  applying  either  of  the  cocaine  methods. 
Cases  of  the  systemic  action  of  cocaine  via  the  pulp  have  been  noted 
in  this  method.  Some  of  these  cases  are  due  to  syncope  alone,  as  it 
has  occurred  when  other  materials  have  been  used  experimentally. 
Hemorrhage  after  the  pulp  extraction  may  be  treated  with  alum  and 
thymol,  or  other  styptic.  If  the  pulp  be  not  exposed,  the  method  is 
useful  to  permit  its  exposure.  A  drop  of  adrenalin,  1  to  1000,  followed 
by  a  drop  of  40  per  cent,  formaldehyde,  pressure  with  raw  vulcanite, 
then  excavation  to  exposure,  then  application  of  ^  grain  of  cocaine  in 
adrenalin  and  formaldehyde,  followed  by  pressure,  has  been  recom- 
mended by  C.  Davis. ^ 

'  Dental  Summary,  1904. 


REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING     469 

G.  A  high-pressure  syringe  may  be  used  in  cases  in  which  the  pulp 
cannot  be  directly  approached.  A  pit  is  made  in  the  dentine  with  a 
No.  ^  bur,  and  the  nozzle  (free  of  air)  of  a  syringe  charged  with  a  15 
per  cent,  solution  of  cocaine  is  steadily  embedded  in  it.  The  force 
exerted  for  several  minutes  charges  the  pulp  with  the  cocaine  solution, 
anesthetizing  it.  If,  after  entry  of  the  dentine  with  a  No.  \  bur,  it  be 
found  still  sensitive,  the  operation  may  be  repeated  or  the  entrance 
enlarged  and  a  new  pit  made.  Care  should  be  taken  not  to  prolong 
the  application  to  too  great  a  degree,  as  after  approach  to  the  pulp 
the  apical  tissue  has  been  profoundly  anesthetized  with  danger  of 
systemic  effect  of  cocaine.  In  one  case,  in  which  repetition  was 
necessary,  the  area  of  apical  tissue  finally  so  anesthetized  accidentally 
included  an  area  of  gum  tissue  one  inch  in  diameter,  which  became 
ischemic.  Some  heart  trouble  developed.  In  case  the  syringe  per- 
mits an  entrance  to  the  pulp,  which  may  be  partially  or  not  at  all 
anesthetized,  it  is  better  to  resort  to  the  other  form  of  pressure 
anesthesia. 

Where  calcific  formations  are  present  they  present  some  difficulty, 
though  with  persistence  one  may  be  enabled  to  anesthetize  the  pulp. 
Cook  recommends  an  application  of  10  per  cent,  sulphuric  acid  for 
a  few  minutes,  followed  hy  sodium  bicarbonate  previous  to  a  reappli- 
cation  of  the  pressure  anesthesia,  as  highly  effective  in  aiding  pene- 
tration of  the  cocaine.^ 

According  to  Brouardel,^  of  Paris,  the  effects  of  cocaine  are  acute 
and  chronic.  The  former  develop  usually  in  ten  or  fifteen  minutes,  or 
ev(>n  u})  to  three-quarters  of  an  hour  after  the  injection.  They  are: 
precordial  anxiety,  filiform  and  extra  rapid  pulse,  lividity  of  the  face, 
coldness  in  the  extremities,  and  abundant  perspiration;  rise  in  tem- 
perature, irregular  respiration,  tingling  sensations  in  the  hands, 
blunted  tactile  sensibility,  excitement,  loquacity,  weeping,  anger,  or 
hysterical  fits;  bilious  vomiting  with  or  without  diarrhea;  anuria, 
symptomatic  epilepsy,  followed  by  motor  and  sensory  paralysis. 
Death  occurs  in  from  two  minutes  to  five  hours  after  administration, 
though  in  the  chronic  cases  fatality  usiudly  does  not  result. 

Placing  the  patient  in  the  horizontal  position,  giving  inhalations 
of  amyl  nitrite,  and,  if  further  cardiac  stimulation  be  necessary, 
hypodermic  injections  of  ether  or  caffeine. 

The  chronic  poisoning  occurs  mostly  in  those  addicted  to  its  use. 
Some  develop  a  tolerance  of  the  drug,  withstanding  from  30  to  120 

'  Dental  Review,  1905.  -  Dental  Cosmos,  U)05,  p.  1508 


470     REMOVAL  OF  DEXTAL  PULP  AND  ROOT-CANAL  FILLING 

grains.     Tachycardia  and  intense  psychic  disturbances,  leading  to 
physical  and  mental  collapse,  are  observed. 

7.  Arkovy  has  recommended  nervocidin  for  its  anesthetic  action 
upon  the  pulp.  A  small  quantity  is  placed  upon  a  piece  of  spunk  and 
applied  to  the  pulp,  which  it  anesthetizes  in  from  a  few  hours  to  a  day, 
when  the  pulp  may  be  painlessly  removed  in  an  ischemic  condition. 
Two  applications  are  required  in  case  of  unexposed  pulp:  one  to 
obtain  a  painless  exposure.^  It  is  not  injurious  to  the  gum.  (See 
p.  367.) 

8.  A  fully  exposed  pulp  in  a  single-rooted  tooth  or  single  root  of  a 
multi-rooted  tooth,  may  be  suddenly  "knocked  out"  by  means  of  a 
delicately  pointed  orange-wood  stick  or  Portuguese  toothpick.  The 
point  is  dipped  in  carbolic  acid  and  suddenly  and  boldly  driven  into 
the  pulp,  either  by  hand  or  mallet  force.  The  method  is  not  so  agree- 
ably delicate  as  pressure  anesthesia,  but  -is  effective.  It  must  not  be 
used  in  partial  exposure,  as,  not  reaching  the  apex,  it  may  cause  pain. 

9.  Darby  uses  with  success  in  deciduous  teeth  a  paste  of  about 
2V  grain  of  cantharides  in  carbolic  acid.  The  application  must  be 
very  carefully  sealed.  Flagg^  mentioned  a  case  of  strangury  in  a 
man  as  the  result  of  its  use  against  a  tooth  pulp.  While  probably  an 
idiosyncratic  case,  the  effect  is  in  correspondence  with  the  known 
occasional  effect  of  cantharides  applied  as  a  vesicant. 

10.  A  vital  remnant  of  pulp  may  be  removed  after  instilling  a 
strong  cocaine  solution,  or  carbolic  acid,  or  a  paste  of  carbolic  acid 
and  acetate  of  morphine,  into  its  substance  by  means  of  a  "puncture 
probe."  This  instrument  may  be  made  by  filing  down  a  Donaldson 
bristle  to  a  fine  point,  which  is  further  whetted  on  an  oil  stone.  The 
sides  of  the  probe  are  polished  by  folding  a  cuttle-fish  disk  upon  itself, 
holding  it  between  the  thumb  and  forefinger  of  the  left  hand,  and 
drawing  the  probe  through  it.  The  pulp  canal  is  flooded  with  the 
carbolic  acid,  and  gentle  thrusts  are  made  into  the  pulp  until  the  probe 
is  stopped  at  the  apex.  If  it  pass  through,  that  must  be  judged  by  the 
sense  of  touch.  At  times  a  sm^ll  end  of  pulp  filament  may  be  seared 
with  a  hot  Evans'  root  drier,  which  is  quickly  thrust  into  it.  This 
does  not  necessarily  give  much  pain. 

1 1.  A  slow  but  effective  method  of  disposing  of  these  filaments, 
when  hyperirritable  or  when  patients  are  timid,  consists  in  packing  a 
cotton  twist  saturated  with  carbolic  acid  containing  cocaine  hydro- 
chlorate  in  solution  into  contact  with  the  pulp  and  then  gently  com- 

'  Soderberg,  Dental  Cosmos,  1901  and  1902.  ^  Private  communication. 


ACTION  OF  ARSENIC  UPON   THE  PULP  471 

pressing  the  pulp.  The  cotton  is  to  be  left  in  position  for  a  day  or 
two,  when,  as  a  rule,  the  pulp  may  l)e  removed.  It  induces  throm- 
bosis, and  carbolic  acid  may  be  used  with  pressure  to  produce  anes- 
thesia at  the  time  of  operation. 

12,  Arsenous  acid  (arsenic  trioxide)  is,  as  a  nde,  prompt,  certain, 
and  complete  in  its  action,  and  is  applicable  for  devitalization  in  nearly 
all  cases  of  pulps  in  mature  teeth.  It  was  introduced  by  Spooner  for 
this  purpose  in  1836. 

When  a  small  quantity  of  pure  powdered  arsenic,  or  of  a  paste  in 
which  it  is  mixed  with  other  ingredients,  is  applied  to  the  pulp  horn 
or  the  dentine,  the  pulp  gradually  dies  progressively  from  the  horn 
toward  the  apex.  So  universally  is  this  the  case  that  a  short  applica- 
tion almost  invariably  involves  the  necessity  of  a  second  application  to 
the  pulp  or  of  a  painful  extirpation  of  the  undevitalized  portion  of  pidp. 

Action  of  Arsenic  upon  the  Pulp. — Arkovy^  was  the  first  to  point  out 
the  details  of  the  action  of  arsenic  upon  the  dental  tissues: 

"  1.  AS2O3  brought  into  contact  with  the  tooth  pulp  acts  in  the 
following  way:  a  certain  degree  of  inflammatory  hyperemia,  total  or 
partial,  depending  upon  the  quantity  of  the  agent  applied,  sets  in; 
the  bloodvessels  become  expanded,  and  here  have  a  tendency  to 
thrombosis.  This  latter  effect  may  also  be  in  connection  with  embo- 
lism of  the  capillaries,  when  the  agent  is  quickly  taken  up  into  the 
bloodvessels. 

"2.  AsjOg  produces  no  coagulation  of  tissue  whatever. 

"3.  It  has  a  specific  influence  upon  the  blood  corpuscles,  combining 
with  the  hemoglobin  to  form  a  compound  of  arsen-hemoglobin,  and 
of  this  chemical  process  there  seems  to  be  evidence  in  the  profuse 
yellowish  tinge  of  the  whole  pulp  tissue  and  in  the  discoloration  of 
blood  in  several  of  the  bloodvessels. 

"4.  In  nearly  every  case  it  is  taken  up  in  substantia  (in  form  of 
molecules)  into  the  blood-ways;  when  there  it  produces,  besides  the 
above-mentioned  changes,  granular  detritus  of  the  contents  and 
anemic  collapse — shrinkage,  the  latter  eft'ect  being  brought  about 
nearly  exclusively  in  cases  where  greater  doses  were  used. 

"5.  The  bulk  of  the  pulp  tissue — viz.,  connective-tissue  fibers  and 
odontoblasts — undergoes  no  change  whatever;  not  so  the  connective- 
tissue  cells,  which  increase  three  or  four  times  their  normal  size. 

"6.  The  special  action  of  arsenic  trioxide  upon  the  nerve  elements 
consists  in  the  following:  the  neurilemma  is  only  so  far  influenced  that 

'  Transactions  of  the  International  Medical  Congress,  London,  1881. 


472     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

its  nuclei  are  somewhat  increased;  a  more  essential  change  takes 
place  in  the  axial  part,  where,  after  the  application  of  more  than  1 
mg.,  granular  destniction  of  myelin  sets  in,  and  the  axis-cylinder 
commences  here  and  there  to  disappear.  A  very  surprising  alteration 
may  be  seen  in  the  notchy  tumefaction  of  the  axis-cylinder,  described 
heretofore  almost  only  in  cases  of  central  lesions. 

"7.  All  these  alterations  occur  in  and  among  nonnal-looking 
tissue. 

"8.  The  action  of  arsenic  trioxide  is  macroscopically  exhibited  by 
a  brownish  red  tingeing  of  the  whole  or  of  certain  parts  of  the  pulp 
body,  as  well  as  of  the  neighboring  dentine  and  the  cementuin,  this 
latter  in  cases  treated  with  greater  doses — ^viz.,  2  to  5  mg.  This 
alteration  is  most  expressed  at  the  top  of  the  crown  pulp  and  at  the 
apical  one-fourth  to  one-third  part.  This  circumstance  may  be 
considered  as  an  external  evidence  of  the  devitalization  being  com- 
pletely attained  to." 

In  some  cases  the  pinkish  discoloration  of  the  dentine  may  be 
marked;  the  broken-down  corpuscles  of  the  extra vasated  blood  have 
their  coloring  matter  taken  up  by  the  odontoblasts,  and  being  dis- 
tributed through  their  protoplasmic  processes  produce  a  condition 
technically  known  as  suffusion.  The  same  result  may  be  an  attendant 
upon  injury  to  the  vessels  from  other  causes,  producing  hyperemia, 
as  when  teeth  are  moved  too  rapidly  in  regulating. 

Miller's  experiments^  upon  the  tails  of  mice  (made  without  and  with 
rings  at  the  root  of  the  tail  to  simulate  the  surroundings  of  the  apical 
vessels  of  a  tooth;  made  without  and  with  encasement  of  the  tails  in 
plaster  of  Paris  to  imitate  the  rigid  surroundings  of  the  dental  pulp) 
showed  that  in  the  alxsence  of  the  plaster  encasement  enormous  edema 
of  tlie  tail  was  produced  and  a  sensory  paralysis  of  the  hind  limbs; 
complete  anesthesia  of  the  tail  occurred  in  forty-eight  hours.  "The 
action  of  arsenic  appeared  somewhat  accelerated  when  a  glass  ring 
was  applied  close  to  the  root  of  the  tail.  In  more  than  forty  cases 
there  was  not  one  in  which  the  action  of  the  arsenic  extended  beyond 
the  ring,  and  the  action  was  not  appreciably  affected  by  enclosing  the 
tails  in  plaster  casts.  The  action  of  the  arsenic  is  of  a  progressive 
nature,  beginning  at  the  point  of  application  and  extending  gradually 
in  each  direction." 

Flagg^  devitalized  ten  pulps  and  removed  them,  cut  off  the  portion 
of  the  bulb  of  each  which  liad  contact  with  the  arsenic,  and  tested  the 

«  Dental  Cosmos.   1894.  2  Ibid.,  1868. 


VARIATIONS  IN  THE  ACTION  OF  ARSENIC  473 

ten  pulps  together  by  Reinsch's  test.  Arsenic  was  found,  estimated  at 
a  one-hundred-thousandth  part  of  a  grain  or  one-milliontli  of  a  grain 
for  each  pulp.  Allowing  for  possible  mechanical  introduction  or 
contact  of  arsenic  during  extirpation,  the  quantity  of  arsenic  intro- 
duced by  the  circulation  must  be  very  minute  indeed. 

Flagg  argued  that,  as  the  pulp  subsequently  putrefies,  it  cannot  have 
died  as  the  result  of  arsenical  poisoning  alone. 

The  indication  is  that  a  minute  quantity  of  arsenic  is  absorbed, 
exerting  its  peculiar  chemical  effects,  which  cause  the  pulp  in  part  to 
become  quickly  filled  with  blood.  Circulation  in  the  part  ceases  and 
death  of  the  part  ensues.  Arkovy's  and  Miller's  experiments  seem  to 
show  that  the  arsenic  may  be  absorbed  into  part  of  the  pulp  beyond 
the  original  area  of  congestion,  and  this  probably  produces  further 
stasis,  which  progresses  apexward.  As  the  apical  pidp  end  dies  it 
induces  a  hyperemic  reaction  in  the  apical  tissue  in  some  cases,  which 
need  not  cause  anxiety,  as  it  generally  passes  away.  It  is  often  relieved 
in  part  by  opening  the  pulp,  which  relieves  the  intense  internal  press- 
ure. Usually  a  sedative  antiseptic  is  applied  .simply  to  prevent 
infection.  The  devitalization  then  becomes  complete,  though  in  some 
cases  the  release  of  pressure  may  cause  a  persistence  of  vitality.  It 
has  been  contended  that  arsenic  may  pass  out  through  the  apical 
foramen.  For  the  roots  with  large  foramina  this  has  been  shown  to  be 
tnie,  as  areas  of  devitalization  of  the  apical  and  overlying  gum  tissue 
have  been  noted.  In  several  apparently  authentic  cases  the  peri- 
cementum of  a  mature  tooth  has  been  said  to  be  destroyed  from  the 
apex  down  and  the  tooth  lost.  I  have  never  seen  such  a  case  resulting 
from  the  arsenical  method  alone  in  either  clinical  or  private  practice, 
although  cases  of  marginal  gum,  alveolar,  and  pericemental  death, 
beginning  as  the  result  of  leakage  or  application  to  perforations,  have 
been  noted.  It  is  probal)le  that  as  stasis  proceeds  the  apical  portion 
of  the  pulp  becomes  involved  in  advance  of  arsenic  absorption. 
Miller's  experiments  show  that  arsenic  does  not  pass  the  point  of 
constriction. 

Variations  in  the  Action  of  Arsenic. — In  most  cases  of  fully  formed, 
single-rooted  teeth  in  young  adults  an  application  of  arsenical  paste 
directly  to  the  exposed  pulp  will  be  followed  by  the  complete  death  of 
the  organ  in  forty-eight  hours.  At  the  expiration  of  that  time  a  steril- 
ized broach  may  be  passed  almost  to  the  apex  of  the  root  and  the  pulp 
removed  en  jnasse  without  pain.  Pulps  of  molars  require  a  longer 
time,  often  a  week,  before  the  filaments  are  dead.     The  finer  filaments 


474    REMOVAL  OF  DEXTAL  PULP  AND  ROOT-CANAL  FILLING 

resist  longer  than  the  larger  ones.  If  pulp  nodules  exist,  the  action 
of  the  arsenic  may  be  delayed  or  in  some  cases  be  almost  nil.  In 
calcareous  and  other  chronic  pulp  degenerations  the  action  is  also 
delayed.  If  arsenical  applications  are  made  over  a  layer  of  dentine, 
the  same  delay  is  noted,  and  is  increased  in  very  mature  teeth.  There 
is  also  a  greater  tendency  to  suffusion. 

Some  pulp,  irrespective  of  the  pulp  condition,  exhibits  a  peculiar 
idiosyncrasy  in  resisting  the  action  of  arsenic,  requiring  large  doses 
and  long  applications  before  succumbing.  Second  applications  often 
require  more  time  to  kill  the  balance  of  the  pulp  than  the  first  appli- 
cation would  have  required.  The  time  used  in  investigation  is  prac- 
tically lost.  The  editor,  therefore,  allows  plenty  of  time;  about  ten 
days  for  molars,  and  prefers  to  find  the  pulp  entirely  dead. 

Forms  in  which  Used. — The  following  formulas  have  been  recom- 
mended. The  analgesics  included  are  intended  to  dilute  the  arsenic 
and  quiet  the  pulp,  and  thus  both  directly  and  indirectly  modify  the 
pain : 

1.  I^. — Acidi  arsenosi, 

Morphinae  sulph aa     gr.  x 

Acidi  carbolici q.  s.  ft.  pasta. — M. 

(J.  D.  White.) 

2.  I^. — Acidi  arsenosi gr.  x 

MorphiniE  acetatis gr.  xx 

Olei  caryophylli q.  s.  ft.  pasta. — M. 

(J    Foster  Flagg.) 
Creosote  may  be  substituted  for  oil  of  cloves. 

3.  I^. — Acidi  arsenosi gr.  x 

Cocainse  hydroch gr.  xx 

Olei  cinnamomi q.  s.  ft.  pasta.  -  M. 

(E.  C.  Kirk.) 

4.  I^. — Arsenic gr.  x 

Alum  gr.  X 

Thymol gr.  x 

Oil  of  cloves    .      . q.  s.  ft.  pasta. — M. 

5.  Any  of  the  above  may  have  the  powdered  ingredients  mixed. 
The  cotton  pellet  may  be  wet  with  an  analgesic  oil  and  then  dipped 
into  the  powder.  Lamp  black  added  to  the  paste  colors  it  so  that  it 
is  easily  distinguishable  in  a  cavity. 

6.  Ab.sorbent  cotton  cross  cut  with  scissors  to  a  fine  lint  may  be 
dusted  into  any  of  the  above  pastes  made  thin  by  adding  an  extra 
portion  of  the  menstruum.  It  is  then  dried  and  bottled  for  use.* 
It  is  calh'd  devitalizing  fiber,  and  offers  less  danger  of  leakage  by 
squeezing. 

'  J.  Foster  Flagg. 


MODE  OF  APPLICATION  OF  ARSENIC  475 

As  the  ordiiiarv  pastes  tend  to  separate  into  layers  of  arsenic, 
morphine,  etc.,  and  nienstrnum  if  made  thin,  they  should  either  be 
made  int(^  stifi"  pastes  or  spread  over  the  bottom  of  a  wide  jar,  so  that 
some  arsenic  may  be  scraped  off  the  bottom  at  each  application. 

Miller  offers  the  following  general  rules  as  deductions  from  his 
observations : 

"1.  The  rapidity  and  intensity  of  the  action  of  arsenous  acid 
depend,  under  certain  circumstances,  to  a  very  considerable  degree 
upon  the  substance  or  substances  with  which  it  is  incorporated. 

"2.  Where  there  is  but  a  small  point  of  exposure,  and  in  particular 
where  extensive  calcification  has  taken  place  in  the  pulp,  escharotics 
should  be  avoided,  since  the  coagulation  of  the  tissue  retards  the 
absorption  of  the  arsenic.  This  retardation  is  but  slight  where  there 
is  a  broad  surface  of  exposure.  In  stubborn  cases,  where  applica- 
tions of  the  ordinary  paste  fail  to  effect  the  devitalization,  a  paste 
consisting  of  arsenous  acid  in  oil  of  cloves,  glycerin,  or  salt  solution 
should  be  employed,  undiluted  by  any  third  constituent. 

"3.  Thymol  is  worthy  of  a  trial  as  a  substitute  for  morphine,  on 
account  of  its  anesthetic  and  antiseptic  properties. 

"4.  For  devitalizing  pulps  of  temporary  teeth  or  remains  of  pulp 
tissue  in  root  canals,  arsenous  acid,  if  employed  at  all,  should  be 
diluted  with  two  or  three  parts  of  some  other  constituent  (thymol, 
zinc  oxide,  morphine,  iodoform)." 

Cobalt  was  introduced  by  Robert  Arthur  as  a  devitalizing  agent 
some  forty  years  ago.  Within  recent  years  it  has  been  employed, 
notably  by  the  Herbst  method  (which  see),  to  destroy  pulps.  The 
colnilt  paste  of  Herbst  was  analyzed  by  E.  C.  Kirk  and  found  to 
consist  of  metallic  arsenic  and  cocaine  hydrochlorate.  Kirk  suggests 
that  free  acids  which  cocaine  salts  may  contain,  or  the  chlorine  from 
the  chloride,  may  combine  with  the  metallic  arsenic  and  form  soluble 
salts.  Commercial  cobalt  will  certainly  devitalize  the  dental  pulp, 
but  it  is  in  consecjuence  of  the  arsenic  contained  in  it. 

Mode  of  Application. — After  sterilization  of  the  cavity  and  pulp  and 
drying,  a  minute  })ellet  of  cotton  is  to  be  rolled  in  the  paste  and  placed 
in  the  desired  location,  or  devitalizing  fiber  used  in  dangerous  ])laces. 
As  arsenic  destroys  gum  tissue  freely,  it  should  be  used  in  minute 
quantity  only,  and  be  accurately  sealed  in  the  cavity. 

In  purely  occlusal  cavities  the  application  may  be  coveretl  with  a 
flat  pellet  of  cotton  containing  an  analgesic,  and  over  this  temporary 
stopping  or  cement  may  be  placed,  or  even  cotton  and  sandarac.     In 


476     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

those  cases  in  which  the  cervical  wall  approaches  the  gum  the  rubber 
dam  should  be  applied,  the  cavity  dried,  and  temporary  stopping 
packed  against  the  cervical  wall,  allowing  it  to  extend  against  the 
adjoining  tooth.  Other  portions  are  packed  into  the  buccal  and 
lingual  walls.  A  pocket  is  thus  formed  into  which  arsenic  may  be 
safely  placed  and  covered  with  a  pellet  of  cotton  containing  an  anal- 
gesic; over  this  may  be  placed  a  last  pellet  of  temporary  stopping, 
which  closes  the  opening.  When  one  is  expert  the  dam  may  at  times 
be  dispensed  with. 

If  the  packing  of  the  temporary  stopping  upon  the  pulp  be  feared, 
a  small  pellet  of  amadou  may  be  laid  over  the  exposure,  and  after 
the  stopping  is  placed  it  may  be  removed. 

The  same  principle  may  be  employed  with  Flagg's  "facing" 
amalgam  or  its  equivalent  alloy  (silver,  40  parts;  tin,  55  parts; 
zinc,  5  parts  plus  mercury). 

It  may  be  used  in  desperate  cases  in  which  no  great  retaining 
periphery  exists  or  where  displacement  by  mastication  is  feared.  In 
its  use  a  pellet  of  spunk  is  laid  upon  the  pulp  and  the  cavity  is  practi- 
cally filled  with  the  soft  amalgam.  An  excavator  is  then  used  to  cut 
through  to  the  spunk,  which  is  carefully  withdrawn.  An  opening  is 
thus  left  into  which  the  application  and  the  extra  cotton  pellet 
saturated  with  the  analgesic  is  placed.  The  opening  is  then  dried 
and  sealed  with  a  portion  of  amalgam.  This  amalgam  will  retain 
its  integrity  for  months,  yet  may  be  removed  in  a  few  minutes  by 
dividing  the  filling  into  two  portions. 

When  pulp  removal  is  intended  the  application  may  be  removed 
through  the  opening  and  a  probe  may  be  passed  into  the  pulp  to  test 
the  progress  of  the  devitalization.  If  needed,  a  second  application 
may  be  made  or  the  tooth  may  be  temporarily  closed.  In  case 
the  pulp  be  found  partially  dead,  it  is  better  to  allow  more  time 
for  complete  devitalization  than  to  make  a  second  application 
(Fig.  392). 

Adhesive  zinc  phosphate  may  be  flowed  over  an  application  if  the 
cavity  be  accessible,  and  oxysulphate  of  zinc  or  even  the  eugenol  and 
zinc  oxide  mixture  may  be  used  as  a  covering.  The  latter  in  cases 
not  permitting  a  "pocket"  is  a  sedative  as  well.  The  saliva  may  be 
admitted  as  soon  as  the  cement  begins  to  stiffen.  Placing  a  small 
portion  of  soft,  quick-setting  cement  upon  a  bit  of  paper  and  carrying 
the  same  to  the  cavity  is  a  valuable  aid  in  preventing  the  tendency 
to  displace  the  arsenic  or  to  draw  away  from  the  part  it  is  most 


MODE  OF  APPLICATION  OF  ARSENIC 


477 


Fig.  392 


desired  to  cover.     If  oiled  paper  he  used,  it  may  later  be  strip})ed  oil' 
if  desired,  or  it  may  be  covered  with  more  of  the  cement. 

The  chief  objection  to  the  placing  of  coverings  after  the  application 
has  been  made  is  the  danger  of  squeezing  the  arsenical  paste,  which 
causes  capillary  attraction  to  quickly  carry  the  arsenic  to  the  cervical 
gum  tissue. 

If  redundant  gum  be  within  the  cavity  of  decay  it  is  to  be  carefully 
saturated  with  trichloracetic  acid  and  cut  away  before  attempting 
to  make  the  arsenical  preparation.  It  has  been  recommended  that 
carbolic  acid  be  always  applied  to  the  gum  margin  to  kill  it.  It  is 
argued  that  arsenic  will  not  pass  through  dead  tissue.^  It  is  better, 
however,  that  no  confusion  of  diagnosis  occur.  If,  after  an  appli- 
cation is  made,  dead  gum  be  found,  it  is 
to  be  presumed  to  have  been  caused  by 
the  arsenic  and  treated  accordingly.  If 
the  coverings  be  made  as  suggested,  the 
danger  of  leakage  is  greatly  lessened. 

If  the  cavity  be  inaccessible,  and  the 
rubber  dam  cannot  be  used  to  exclude 
fluids,  and  an  arsenical  application  can- 
not be  made  with  precision,  or  when 
arsenic  applied  directly  is  likely  to  cause 
pain,  it  is  advisable  to  form  a  special 
cavity  or  "pocket"  for  its  reception. 
This  should  always  be  made  when  pos- 
sible in  a  line  of  direct  approach  to  a 
healthy  pulp  horn.  The  cavity  is  to  be  made  as  deep  as  possible 
without  plunging  into  the  pulp.  A  spear  drill  of  narrow  face  is  to  be 
used.  In  some  cases  two  or  more  applications  of  the  paste  are 
required;  as  soon  as  the  pulp  can  be  exposed,  a  direct  application  of 
the  paste  is  to  be  made.  If  rapidity  of  devitalization  is  not  an  object 
it  may  be  left  against  the  dentine  of  the  pocket  for  some  time.  The 
cavity  of  decay  is  used  as  a  receptacle  for  analgesics  in  these  cases. 

Cervical  cavities  not  having  a  retentive  form,  and  abraded  teeth, 
otter  difficulties,  which  are  overcome  by  drilling  a  pocket  for  the 
reception  of  the  paste. 

In  cases  where  there  are  pulp  nodules,  and  where  chronic  degen- 
erations of  the  pulp  exist,  the  arsenic  is  removed  at  the  end  of  the 
usual  devitalizing  period  and  free  entrance  is  made  to  the  pulp. 


DiaKiani  .-howiriK  mrtiuid  (if  fir.-t 
making  Uie  (•()\eiiiiK  for  an  arseni- 
cal or  sedative  application.  (See 
te.xt.)  EP.  e.xposed  pulp;  AA, 
arsenical  application;  C,  sedative 
covering  to  same;  A,  amalgam 
placed  before  the.se  applicati(jns: 
-l',  amalgam  to  seal  them  in;  f, 
enamel. 


'  Clowes. 


478     REMOVAL  OF  DEXTAL  PULP  AND  ROOT-CANAL  FILLING 

cutting  away  all  insensitive  portions;  if  pulp  nodules  can  be  lifted 
away  painlessly,  they  are  removed,  and  a  fresh  application  of  arsenic 
is  made,  to  remain  again  several  days.  In  all  of  these  cases,  to 
effectually  devitalize  it  may  be  necessary  to  apply  a  paste  of  arsenic 
trioxide  in  glycerin,  or  in  one  of  the  essential  oils. 

Before  applying  the  arsenic  to  the  pulp  the  latter  is  always  to  have 
been  quieted  and  its  superficies  sterilized. 

During  the  application  all  pressure  is  to  be  avoided  or  inflammation 
will  be  induced,  which  defeats  the  absorption  of  the  arsenic  and 
causes  needless  pain  as  well. 

If  the  pulp  be  much  diseased  at  the  point  of  exposure,  it  is  better 
to  apply  the  arsenic  to  healthy  dentine  at  another  portion  of  the 
cavity,  or  in  a  pocket,  and  apply  analgesics  at  the  point  of  exposure. 

Symptoms. — ^A  vast  majority  of  pulps  die  with  no  more  pain  than 
the  slight  sensation  of  throbbing  or  fulness  due  to  the  gradual  and 
rapid  production  of  bulbar  stasis.  In  these  cases  the  absorption  of 
the  arsenic  has  been  prompt  and  the  irritative  effects  less  than  the 
paralyzant.  In  some  cases  the  throbbing  pain  may  be  felt  shortly 
after  application,  and  may  pass  away  rapidly.  In  others  the  appli- 
cation must  be  removed  and  the  pulp  quieted  before  the  end  of  the 
sitting  or  a  day  or  two  later.  In  others,  again,  the  pain  may  begin 
several  hours  after  application,  and  either  pass  promptly  into  the 
sensation  of  heavy  fulness  or  it  may  become  paroxysmal.  If  endured 
for  about  two  hours,  this,  as  a  rule,  gradually  or  suddenly  ceases. 
If  applied  to  healthy  dentine  in  sound  teeth,  the  pain,  if  any,  will 
be  delayed,  and  if  applied  to  sound  dentine  of  teeth  which  have  pulps 
elsewhere  exposed,  little  pain  is  produced  if  the  pulp  be  kept  under 
the  influence  of  an  analgesic. 

In  some  cases  apical  pericemental  hyperemia  supervenes,  with 
elongation  of  the  tooth.  This  will  pass  away  spontaneously,  or  if 
the  tooth  be  guarded  (see  Acute  Apical  Abscess)  and  iodine  applied 
to  the  gum  as  a  counterirritant. 

Not  infrequently  when  the  arsenic  is  applied  to  the  dentine, 
whether  for  twenty-four  hours  or  longer,  the  pain  and  suffusion  of 
venous  hyperemia  may  occur.  It  may  be  relieved  by  opening  the 
pulp,  even  though  it  should  not  bleed.  A  sedative  is  then  to  be 
applied.     The  pulp  may  then  die  under  this  sedative. 

In  cases  of  secondary  dentine  or  nodules  pain  may  supervene,  no 
matter  whether  the  arsenic  be  applied  to  the  dentine  or  the  pulp. 
The  amount  of  pain  produced  seems  to  depend  more  upon  the  con- 


ACCIDENTS  WITH  ARSEXIC  479 

dition  of  the  pulp  than  upon  other  considerations.  Vigorous,  healthy, 
and  diseased  pulps  are  apt  to  respond  to  arsenic.  It  is  assumed  that 
absorption  is  incomplete. 

In  some  cases  intense  pain  is  produced,  which  may  be  relieved  by 
opening  the  pulp  and  ap[)lying  a  sedative.  Often  simple  removal  of 
the  covering  and  the  application  gives  relief,  so  that  pressure  pain  is 
the  diagnosis.     It  may  not  appear  until  the  pulp  is  nearly  all  dead. 

Accidents  with  Arsenic. — If  .a  portion  of  an  arsenical  application 
escape  from  beneath  its  covering,  it  may  destroy  much  or  a  little  gum 
tissue,  according  to  the  amount  which  escapes. 

The  arsenic  may  attack  the  gum  festoon,  inducing  in  it  stasis 
followed  by  necrosis.  The  gum  assumes  a  purplish  turgidity,  which 
later  changes  to  a  dirty  yellow  slough. 

The  bone  is  usually  devitalized  for  a  distance. 

If  the  necrosis  be  self-limited,  as  is  usually  the  case,  a  small  seques- 
trum comes  away  after  a  few  weeks. 

In  some  cases  the  arsenic  may  follow  the  festoon  of  the  gum  of  one 
or  more  teeth,  causing  disagreeable  sloughs  and  ulcerations.  It  may 
follow  the  pericemental  tract,  kill  the  pericementum,  and  the  tooth 
drops  out.  The  alveolar  process  about  one  or  several  teeth  may  be 
devitalized  and  a  sequestrum  occur  which  includes  the  teeth.  Certain 
toothache  nostnims  are  sold  which  contain  arsenic.  Dr.  G.  C. 
Chance^  records  a  case  of  arsenical  necrosis  occurring  from  this  source. 
Dr.  J.  E.  Powers'  records  a  case  in  which  extensive  necrosis  occurred 
from  the  use  of  colored  woollen  yarn  (as  a  cleanser  of  interdental 
spaces)  which  contained  arsenic  used  in  the  dye. 

From  the  infirmary  of  the  Philadelphia  Dental  College  was  referred 
to  the  oral  clinic  a  case  of  extensive  coagulation  necrosis,  resulting 
from  the  rubbing  of  "toothache  drops"  upon  the  gum.  Analysis 
showed  the  preparation  used  contained  arsenic.  Collapse  from  blood 
poisoning  being  the  immediate  danger,  the  child  was  operated  upon 
by  Prof.  Boenning  for  drainage  of  the  parts.  During  the  recovery, 
the  teeth  from  the  right  lower  cuspid  to  the  left  lower  second  temporary 
molar,  and  the  gums  over  the  process,  were  lost,  leaving  a  blackened 
alveolar  process,  to  be  later  removed  surgically  (Fig.  o93). 

Arsenic  is  liable  to  pass  through  the  apical  foramina  of  unformed 
or  much  resorl)ed  roots.  It  may  possibly  pass  through  mature  roots 
when  an  application  is  placed  high  u{)  in  the  canal,  rarely  when  ajiplicd 

'  Proceedings  of  the  Academy  of  Stomatology.  Philadelphia.   1898. 
-  International  Dental  Journal,  November,  1902. 


480     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

under  normal  conditions  (as  recorded  by  some),  or,  as  occurred  in  one 
case,  by  the  application  being  pushed  through  the  apex.  It  may  be 
forced  through  in  the  act  of  broaching,  or  through  the  subsequent  use 
or  the  cataphoric  current  or  pressure  anesthesia  without  the  prelimi- 
nary precaution  of  removing  the  arsenic. 

In  some  cases  arsenic  has  been  applied  to  perforations  made  through 
the  sides  of  foots  under  the  impression  that  the  vital  tissue  found  was 
pulp  tissue.  In  such  case  its  necrotic  effects  will  be  noted  upon  the 
gum  overlying  the  root  apex  or  over  the  perforation,  the  tooth  being 
loosened  and  extruded  and  may  possibly  be  lost. 

E.  C.  Kirk^  has  recorded  several  cases  of  loss  of  teeth  from  arsenical 
necrosis  of  the  pericemental  tissue  following  the  use  of  mummifying 

Fig.  393 


Boenning's  case  of  coagulation  necrosis  due  to  arsenic;   shows  exposed  and  blackened 

alveolar  process. 

paste  to  pulp  stumps  previously  impregnated  with  arsenic.  His 
theory  is  that  the  arsenic  was  liberated  by  the  affinity  of  the  ingredients 
of  the  mummifying  paste  for  the  proteid  constituents  of  the  pulp 
tissue. 

Such  flangers  as  these  demand  that  extreme  precautions  be  taken 
against  the  careless  use  of  quantities  of  the  agent.  The  rules  laid 
down  should  be  adhered  to. 

The  only  cure  of  the  condition  consists  in  the  thorough  removal  of 
every  particle  of  the  arsenic.  Any  projecting  masses  of  edematous 
gum  should  be  cut  away,  as  they  are  dead  and  will  slough  at  any  rate, 
and  a  freer  access  to  deep  parts  is  had — the  blood-flow  may  itself  wash 

I  Dental  Cosmos,  October,  1903. 


REMOVAL  OF  THE  PULP  481 

away  the  arsenic.  The  forcible  washing  should  be  prolonged  and 
repeated.  Dialyzed  iron  or  tincture  of  iodine  should  be  applied  with 
a  view  to  possible  neutralization  of  the  arsenic. 

The  editor,  in  a  case  of  known  application  of  arsenic  to  an  obscure 
perforation,  succeeded  in  causing  regeneration  of  tissue  by  removing 
surgically  the  dead  tissue  and  inviting  regeneration. 

It  may,  therefore,  be  that  after  minute  portions  of  arsenic,  forced 
through  foramina,  exert  their  full  effect,  the  resulting  dead  tissue  may 
be  removed  by  resorption  or  even  exfoliation;  indeed,  this  result  has 
been  noted  in  which  no  other  explanation  seemed  possible. 

If  the  teeth  are  loosened  and  lost  as  the  result  of  arsenical  necrosis, 
either  beginning  at  the  gum  margin  or  at  the  apical  space,  the  alveolus 
will  exhibit  a  bare  periphery  and  even  some  odor  of  putrefaction  may 
be  present.  The  alveolus  should  be  sterilized  and  the  walls  burred 
away  to  a  tissue  capable  of  healthy  granulation. 

If  suffusion  occur,  essential  oils  or  phenol  should  be  avoided  in  the 
subsequent  treatment,  as  they  tend  to  set  the  color  by  acting  as  a 
mordant  (Kirk),  rendering  bleaching  difficult.  After  the  pulp  is 
removed  it  is  well  to  fill  the  apical  portion  of  the  canal,  and  then  at 
once  bleach  with  25  per  cent,  ethereal  pyrozone,  after  which  the  balance 
of  the  canal  and  the  cavity  may  be  filled.  (See  Moist  Gangrene  of 
the  Pulp.) 

REMOVAL  OF  THE  PULP. 

At  the  end  of  four  or  five  days,  in  single-rooted  teeth,  ten  days  in 
multi-rooted  teeth,  the  dressing  seals  and  cotton  containing  the  paste 
are  removed,  the  cavity  freely  washed  with  hydrogen  dioxide,  and 
the  rubber  dam  applied.  Large,  sterilized  rose  burs  are  used  to  open 
the  pulp  chamber  freely  and  to  remove  all  softened  dentine. 

The  cavity  is  now  to  be  given  such  form  that  pulp  broaches  may  be 
passed  directly  and  freely  to  the  apex  of  each  root.  This  rule  is  to  be 
followed,  no  matter  how  much  tooth  substance  is  sacrificed  to  carry  it 
into  effect.  As  the  future  health  of  the  tooth  depends  almost  entirely 
upon  the  thoroughness  with  which  each  canal  is  cleansed,  sterilized, 
and  hermetically  sealed  at  the  apex,  it  is  evident  that  the  removal 
of  crown  tissue  is  a  small  evil  compared  with  incomplete  entrance 
to  and  cleansing  of  a  canal.  This  is  also  to  be  done  immediately 
after  cocainization. 

A  new  and  perfect  pulp  broach  is  dipped  in  carbolic  acid  and  gently 
31 


482     REAIOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

passed  to  the  apex  of  the  root;  the  teeth  of  the  broach  are  turned  away 
from  the  pulp  until  the  instrument  is  fully  inserted,  when  the  broach 
is  turned  so  that  its  teeth  shall  engage  the  entire  length  of  the  pulp, 
which  may  then  usually  be  removed  entire.  The  finest  Donaldson 
cleanser  may  sometimes  be  used  in  almost  this  manner.  Cotton  may 
be  wound  on  a  fine  Swiss  broach  and  twisted  into  the  pulp  to  engage  it. 

In  multi-rooted  teeth  the  largest  canal  may  have  its  pulp  removed 
as  above  indicated.     As  a  rule,  the  smaller  canals  require  enlargement. 

A  small  bud-drill  should  be  passed  into  the  mouths  of  canals,  slightly 
enlarging  them.  Kerr  or  Downie  broaches — a  form  of  tapering 
twist  drill— are  then  pushed  with  a  twisting  motion  into  the  canals  as 


Fig.  394 


Fig.  395 


Kerr  root-canal  reamers  and  broaches. 


Downie  root-canal  reamers  and  broaches. 


far  as  they  will  go  and  turned,  reaming  the  canal.  As  they  are  of  fine 
temper  and  the  smaller  sizes  conform  to  the  curve  of  the  canal,  they 
are  comparatively  safe.  The  smallest  is  used  first,  then  the  larger 
ones.  They  may  also  be  had  for  the  straight  and  angle  hand  pieces. 
Successive  sizes  of  nicely  tempered  Swiss  broaches  may  be  used  as 
canal  reamers  until  larger  instruments  can  be  used.  Of  these,  the 
writer  prefers  the  Downie  broaches  (Fig.  395). 

Gates-Glidden  or  Walker  drills  may  be  used  or  Donaldson  cleansers 
may  be  employed  to  rasp  the  sides  of  the  canal  not  touched  by.  the 
Downie  or  Swiss  broaches.  They  are  introduced  into  the  canal  to  thefull 
depth  possible,  and  then  brought  out  with  a  spring  bearing  against  the 
wall  to  1)6  rasped.     If  the  canal  be  wet  with  a  5  per  cent,  formalin 


REMOVAL  OF  THE  PULP 


483 


solution  or  other  antiseptic,  the  pulp  is  also  comminuted  and  washed 
down  toward  the  pulp  chamber. 

In  place  of  drills  the  process  of  canal  enlarj^enient  devised  by  Calla- 
han^ may  be  employed.  The  general  cavity  wall  is  varnished  to 
prevent  the  action  of  the  acid  upon  the  dentine,  and  by  means  of  a 
pair  of  Flagg's  dressing  pliers  or  a  minim  dropper  a  drop  of  sulphuric 


Fig.  396 


Fig.  397 


Fig.  398 


Fig.  399 


i 


Dr.  Donaldison's  pulp-canal  cleansers. 


acid  (50  per  cent,  solution)  is  deposited  at  the  mouth  of  the 
canal  to  be  operated  upon.  The  finest  size  of  Donaldson's 
canal  cleanser  is  then  passed  into  the  canal  as  far  as  it  will 
go,  using  a  pumping  movement  to  carry  the  acid  farther  into 
the  canal  and  to  scrape  the  canal  walls  softened  by  the  action 
of  the  acid.  The  acid  chemically  destroys  any  organic 
matter — i.  e.,  pulp  tissue — present,  releases  the  calcium  of 
the  dentine  from  its  combination,  and  forms  calcium  sul- 
phate, which  is  mechanically  removed  by  scrapers.  Care 
must  be  observed  not  to  strain  the  broaches  too  greatly,  as 
they  may  break.  The  operation  is  continued  until  the  apex 
of  the  root  is  reached.  F.  T.  Hayes  suggests  the  use  of  aqua 
regia  as  less  injurious  to  broaches;  lactic  acid  is  also  less  injurious. 
When  the  clean.ser  will  not  enter  readily  it  is  well  to  file  away  the 
barbs  from  an  old  clean.ser  and  leave  it  roughened,  and  to  u.se  it  for 
a  time  with  the  acid  until  the  cleanser  proper  can  be  employed. 
Iridioplatinum  or  gold  broaches  may  be  used  for  this  purpose. 

In  the  canals  of  posterior  teeth  short  cleansers  are  mounted  in  a 


•  Proceedings  of  the  Ohio  State  Dental  Society,  1894. 


484     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

chuck  handle  and  the  shank  sharply  bent  at  a  right  or  obtuse  angle. 
If  the  cleanser  bind  in  the  canal,  it  should  be  grasped  with  the  thumb 
and  forefinger  and  given  a  straight  pull  to  relieve  it. 

The  use  of  5  per  cent,  formalin,  tannin,  or  alum,  to  be  specially 
applied  about  two  days  after  the  application  of  arsenic,  has  been 
suggested  for  the  toughening  of  pulps.  Their  use  necessitates  a  visit 
for  their  special  application.  They  toughen  the  pulp,  and,  while  the 
advantage  in  pulp  removal  is  offset  by  the  special  visit  needed,  may, 
in  fine  canals,  mummify  inaccessible  portions  of  pulp  tissue. 

The  point  of  importance  is  the  removal  from  the  pulp  canal  of  all 
removable  portions  of  pulp  tissue  and  an  enlargement  sufficient  to 
admit  a  satisfactory  root  filling.  It  is  an  open  question  whether  in 
multi-rooted  teeth  this  is  ever  complete,  or  whether  it  is  necessary  that 
it  be  made  absolutely  so,  regardless  of  other  dangers. 

A  perfectly  safe  rule  for  mechanical  procedures  is  as  follows :  Use 
drills  only  when  they  advance  readily  into  the  root  lumen;  prefer 
Downie  broaches  and  Donaldson  cleansers  under  other  circumstances. 
Advance  no  large  reamers  into  delicate  apical  portions  of  roots,  as  a 
lateral  perforation  may  be  made.  If  a  fine  broach  cannot  be  passed 
through  the  apical  foramen,  do  not  attempt  its  enlargement;  and 
it  is  better  to  preserve  a  normal  foramen,  as  large  foramina  present 
greater  difficulty  of  filling  than  normal  ones. 

If  doubt  exist  as  to  the  presence  of  a  portion  of  pulp  in  the  apex 
of  the  root,  papain  paste  may  be  placed  in  the  canals  for  a  few  days 
to  digest  the  remaining  pulp  tissue.    (See  Pulp  Digestion.) 

If  the  pulp  be  removed  as  far  as  possible  by  careful  work  and  the 
canal  sealed  to  that  point  with  a  mechanically  perfect  and  antiseptic 
root  filling,  it  is  improbable  that  any  future  trouble  will  arise,  and  it  is 
better  that  any  such  trouble  should  be  subsequently  treated  than  that 
immediate  trouble  should  be  set  up  by  perforation  in  an  endeavor  to  force 
a  finding  of  canals  which  a  very  fine  Downie  or  Kerr  cleanser,  or 
broach,  will  not  explore. 

It  has  been  recommended  that  all  canals  should  be  drilled  or  scraped 
to  remove  the  organic  matter  attached  to  the  periphery  of  the  dentine. 
Such  organic  matter  may  later  undergo  putrefaction,  and  is  removed 
\)y  the  above  method. 

If  the  operations  have  been  done  under  antiseptic  precautions,  the 
root  is  ready  for  filling,  unless  irritation  of  the  apical  tissues  be  severe, 
in  which  case  a  sedative  antiseptic — e.  g.,  menthol  in  chloroform — on 
cotton  should  be  sealed  in  the  canal.    The  gum  should  be  painted  with 


THE  ROOT-CANAL  FILLING  485 

iodine  as  a  counterirritant  and  the  subsidence  of  the  symptoms 
awaited.     (See  Aseptic  Apical  Pericementitis.) 

Rhein  recommends,  for  the  treatment  of  inaccessible  portions  of 
recently  devitalized  pulps,  the  use  of  a  chemically  pure  zinc  point  to 
be  placed  in  the  root  moistened  with  a  1  to  500  mercuric  chloride  in 
hydrogen  dioxide  (3  percent,  solution),  and  the  anode  of  the  cataphoric 
appliance  applied  to  it,  the  cathode  sponge  to  be  placed  under  the 
dam  on  the  cheek.  From  1  to  5  milliamperes  of  current  are  used 
and  maintained  for  from  three  to  seven  minutes  according  to  the 
exigency. 

Zinc  oxychloride  is  produced  and  carried  into  the  tissue. 

It  is  always,  perhaps,  safer  to  introduce  a  sealed  dressing  of  phenol 
camphor  plus  menthol  or  thymol  until  all  possible  hemorrhage  or 
irritation  has  subsided.  In  case  of  pressure  anesthesia  with  free  hem- 
orrhage, a  little  alum  and  thymol,  equal  parts,  is  well  added  to  the 
phenol  camphor,  or  even  a  dry  dressing,  to  absorb  any  secondary 
hemorrhage  (Ottolengui). 


THE  ROOT-CANAL  FILLING. 

The  features  to  be  possessed  by  a  canal  filling  are  the  following: 
(1)  It  should  be  non-irritating;  (2)  it  should  hermetically  seal  the 
canal;  (3)  it  should  be  unalterable  in  the  conditions  surrounding 
it;  (4)  if  possible,  it  should  be  continuously  antiseptic,  and  (5)  be 
removable  if  subsequent  conditions  ever  demand  its  removal. 

These  conditions  may  all  be  fulfilled  in  the  well-opened  roots  by 
the  use  of  temporary  stopping  or  wax,  each  made  antiseptic  by  com- 
bining with  it  suitable  ingredients.  Each  may  be  gently  melted  in  a 
spoon  held  over  a  flame  and  a  third  of  its  bulk  of  aristol  or  iodoform 
incorporated  with  it.  When  partly  cold  it  is  moulded  into  cones 
suitable  for  introduction  into  the  canal.  This  may  be  done  on  a  glass 
slab  by  rolling  with  an  ivory  paper-cutter  or  spatula.  When  the  canal 
is  prepared  and  its  w^alls  thoroughly  dried  by  means  of  hot  air,  a  trifle 
of  eucalyptol  is  introduced  into  the  canal  and  all  excess  removed,  or  a 
little  chloropercha'  is  introduced.  The  pointed  section  of  a  cone  of 
temporary  stopping  or  gutta-percha  is  attached  by  heat  to  a  canal 
plugger  and  carried  to  the  apex  of  the  canal,  where  it  is  firmly  \^i 

1  Chloropercha  is  a  solution  of  guttu-peicha  in  chloroform;  aristolf  iodoform,  or  hydro- 
naphthol  may  be  added.  If  it  has  hardened,  add  chlcroform  and  place  in  a  dish  of  hot 
water  to  hasten  solution.     Dental  Office  and  Laboratory,  1907. 


486     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

gently  compressed.  Other  sections  are  added  until  the  canal  is  one- 
half  or  three-quarters  filled.  Over  this  is  placed  oxychloride  of  zinc  or 
zinc  phosphate  made  antiseptic  by  the  addition  of  hydronaphthol 
while  mixing  (Fig.  400).  Whether  the  crown  filling  shall  be  intro- 
duced at  the  same  sitting  or  not  depends  upon  the  general  irritability 
of  the  tissues  of  the  patient  and  the  operator's  convenience.  As  a 
rule,  it  is  well  to  temporarily  fill  the  crown  cavity  with  base-plate 
gutta-percha/  apply  a  good  counterirritant  to  the  gum  over  the  apex, 
and  permit  the  apical  tissues  to  recover  their  normal  tone.  In  a  vast 
majority  of  cases  this  immediate  root  filling  is  accompanied  by  a  suc- 
cessful issue,  whether  some  apical  irritation  arise  or  not,  and,  as  a  rule, 
it  does  not  amount  to  much. 

In  case  of  an  open  foramen  a  long  cone  is  rolled;  this  is  tried  in  the 
canal,  and,  passing  through  the  foramen,  will  irritate  the  tissue.    It  is 


Fig.  400 


Fig.  401 


Root-canal  filling:  A,  gutta-percha; 
B,  oxychloride  of  zinc. 


A,  perforation  through  side  of  apex;  D,  cone  of 
gutta-percha  passing  through;  B,  portion  to  be 
cut  off;  C,  jiortion  of  canal  not  treated. 


cut  oft'  a  line  at  a  time  until  it  stops  at  the  foramen  without  irritation. 
To  allow  for  slipping  of  the  cone,  a  half-line  more  is  removed.  The 
apex  of  the  canal  is  moistened  with  thick  antiseptic  chloropercha  and 
one-quarter  inch  of  cone  packed  into  the  root  canal,  which  it  should 
exactly  fit  (Fig.  401).  A  bit  of  sterilized  grafting  sponge  may  be 
inserted  beyond  the  apex  and  the  canal  then  filled.  A  neat  method  of 
measuring  the  cone  is  to  use  a  very  fine  and  short  Donaldson  hook. 
This  is  passed  through  the  perforation,  or  open  canal  end,  and  explores 
its  characteristics.  A  bit  of  rul)ber  dam  slipped  upon  the  shank  is 
pushed  up  to  some  guide  point,  say  the  incisal  edge,  while  the  hook  is 
held  against  the  apical  canal  edge.  This  gives  the  exact  length 
between  these  points.  The  cone  is  now  tried,  until  it  no  longer 
irritates  yet  fits  the  apical  foramen,  and  the  guide  point  level  marked 


'  White  base-plate  gutta-percha  may  now  be  had. 


THE  ROOT-CANAL  FILLING  487 

upon  it.  Measuring  from  the  point  on  the  cone  by  placing  the  rul)ber 
dam  mark  upon  it,  the  lower  side  of  the  hook  marks  the  apical  edge 
of  the  root.  Allow  for  slipping  if  a  section  of  cone  is  to  be  used,  or 
press  the  cone  into  the  canal,  moistened  with  thick  chloropercha  until 
the  mark  is  at  the  guide  point.  Cut  off  the  cone  inside  the  pulp  cham- 
ber with  a  hot  instrument,  heat  the  cone  with  hot  air,  and  gently  pack 
into  the  canal. 

In  the  case  of  wax,  yellow  beeswax  and  aristol  or  wax  and  paraform 
are  to  be  preferred  to  paraffin.  The  cone  is  thrust  into  a  dry  canal, 
packed  cold  for  a  distance,  and  then  the  point  of  a  warmed  Evans 
root  drier  is  used  to  melt  and  pump  it  into  the  canal  until  the  latter 
is  partly  filled,  when  oxychloride  of  zinc  or  antiseptic  zinc  phosphate 
is  used  to  cover  it. 

In  open  canals  thin  oxychloride  of  zinc  may  be  introduced.  It  is 
carried  to  place  upon  shreds  of  cotton.  Some  operators  prefer  to 
place  a  shred  of  cotton  saturated  with  an  antiseptic  oil  in  the  apex 
of  the  root  canal.  It  has  been  claimed  that  the  cotton  is  converted 
into  amyloid.  I  have  conducted  experiments  to  determine  this  point, 
and  found  that  it  can  hardly  be  true  for  oxychloride  of  zinc,  although 
tme  when  cotton  is  placed  in  a  chloride  of  zinc  solution. 

Good  results  are  nevertheless  obtained  by  the  method,  owing  to  the 
antiseptic  property  of  the  oxychloride  of  zinc.  It  is  very  difficult  of 
removal,  and  should,  therefore,  only  be  employed  after  temporarily 
dressing  the  canal  with  a  sedative  antiseptic,  unless  it  be  desired  to 
take  the  risk  of  apical  pericementitis,  which,  in  these  cases,  is  a  rare 
sequel.  A  slight  degree  of  moisture  at  the  apex  is  an  advantage,  as 
it  mixes  with  the  material  and  permits  a  flow  to  the  apex. 

Antiseptic  chloropercha — a  solution  of  gutta-percha  in  chloroform 
with  aristol  or  iodoform  added — may  be  used  on  a  twist  of  cotton  as  a 
filling  in  place  of  a  cone.  It  is  more  difficult  of  removal  than  the 
cone,  owing  to  the  presence  of  the  cotton  fibers.  Ottolengui  recom- 
mends that  a  number  of  pieces  of  floss  silk  about  an  inch  long  be 
saturated  with  chloropercha  and  dried.  These  are  to  be  introduced 
into  the  previously  placed  chloropercha  and  the  end  allowed  to  remain 
in  the  pulp  chamber.  If  removal  be  necessary,  the  floss  may  be 
engaged  and  removed.  If  a  root  can  be  drilled  for  a  free  opening, 
the  gutta-percha  cone  can  largely  be  removed  with  the  drill. 

In  the  finer  canals  an  antiseptic  eucalyptol  solution  of  gutta-percha 
is  preferable  to  chloropercha.  Dr.  J.  C.  Blair  has  introduced,  under 
the  name  of  "  Forma-Percha,"  such  a  solution  containing  oil  of  cassia 


488      REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

and  paraform.  Its  uses  as  a  root  filling  are  identical  with  those  of 
chloropercha.  Its  removability  lies  in  its  weakness  of  cohesion 
after  drying.  For  use  it  should  be  warmed  into  a  creamy  mass  and 
used  with  cotton/  or  pressed  into  the  canal  and  a  cone  of  gutta-percha 
or  temporary  stopping  introduced.  B.  L.  Cochran^  offers  the  follow- 
ing rational  formula,  making  an  analogous  material: 

I^. — Gutta-percha  base  plate §  S3 

Dissolve  in  chloroform q.  s.  to  thin  solution. 

Add  saturated  solution  of  thjrniol  in  oil  of  eucalyptus,  f  5ss.  Let  the  chloroform  evaporate. 
Dr.  Roth  also  adds  hydronaphthol. 

Raw  cotton  with  wood  creosote  has  been  used  for  the  finer  canals, 
but  cotton  is  an  absorbent,  and  after  losing  the  creosote  may  take 
up  deleterious  matter  unless  mechanically  antiseptic  coverings  are 
placed  over  it.  If  used  alone,  at  all,  it  should  be  confined  to  the 
apical  third  of  doubtful  roots.  With  oxychloride  of  zinc,  chloro- 
percha, or  other  impervious  materials  in  its  meshes,  cotton  is 
probably  a  root  filling  of  more  permanency.  An  excellent  material 
with  which  to  saturate  it  is: 

IJ. — Paraform 1  part 

Thymol    .      ,      .      .• 2  parts 

Alum 1  part 

Oxide  of  zinc 2  parts 

Creosote q.  s.  to  a  thick  or  thin  paste. 

This  is  highly  antiseptic,  and  reasonably  permanent. 

The  obloquy  which  has  attached  to  cotton  has  been  due  to  its  use 
with  a  simple  oil  too  close  to  leaky  fillings,  which  have  permitted  it  to 
absorb  infective  material,  or  its  use  in  poorly  cleansed  canals.  In 
proper  use  some  of  the  incorporated  material  should  be  run  into  the 
canal  in  advance  of  it,  and  the  surplus  should  be  condensed  over  its 
coronal  end.  Introduced  on  Swiss  broaches  it  carries  the  filling 
material  to  fine  root  ends  with  great  accuracy. 

The  secret  of  success  in  root-canal  filling  lies  perhaps  more  with  the 
prevention  of  infection  from  the  mouth  than  with  the  character  of 

'  When  cotton  is  used  as  a  root  filling  or  a  vehicle  for  non-absorbent  substances  it  should 
be  mounted  on  a  delicate  Swiss  broach  tapering  nicely  from  shank  to  point,  which  should  have 
its  hard  temper  drawn  by  annealing  in  a  test-tube  over  a  flame.  The  heat  is  applied  at  the 
shank,  and  the  tube  is  to  be  moved  over  the  flame  so  that  a  pigeon-blue  color  runs  out  to  the 
tip  of  the  blade.  Such  broaches  are  fit  for  reamers,  and  are  of  splendid  temper.  The  tip  should 
be  removed  with  scissors,  so  that  penetration  of  the  cotton  may  be  avoided.  The  wisp  of  cotton 
it  to  be  laid  upon  the  left  forefinger,  the  broach  laid  upon  it,  the  thumb  closed  down,  and  the 
broach  twisted  with  the  right  thumb  and  forefinger,  the  left  ones  Ijeing  then  used  to  stroke  the 
cone  to  symmetrical  form.  This  requires  some  practice.  As  a  swab  this  is  always  twisted 
to  the  right.  An  a  dressing  it  is  passed  into  the  root,  twisting  to  the  right.  When  placed,  the 
broach  is  given  two  turns  to  the  left,  is  .slightly  withdrawn,  and  then  pressed  in  again.  This 
oau.ses  tlie  cotton  to  be  crimjjed  upon  it.self.  Raw  cotton  is  preferable  to  absorbent  when  used 
for  other  purposes  than  as  a  root  swab.     A  slight  excess  at  the  end  may  be  cut  or  burned  off. 

2  Dental  Review,  1905. 


THE  ROOT-CANAL  FILLING  489 

the  material  placed  in  the  apex  of  the  root  canal.  Nevertheless,  the 
prevention  of  ingress  of  fluids  from  the  apical  tissues  seems  to  he 
necessary;  at  least  the  entrance  of  such  fluids  invites  earlier  infection. 

While  recurrent  sepsis  may  arise  by  way  of  the  circulation,  exj)e- 
rience  with  my  own  canals  and  those  of  others  leads  me  to  doubt  its 
frequency  as  a  cause.  Opportunity  for  oral  infection  is  usually  suffi- 
cient, as  absolutely  tight  fillings  are  difficult  to  make. 

There  is  no  objection  to  the  use  of  removable  fillings  if  they  are 
mechanically  and  antiseptically  perfect.  There  is  no  necessity  to  use 
them  in  all  cases  from  timidity,  as  in  many  roots  the  fillings  more 
difficult  of  removal  are  indicated. 

Accidents  Occurring  during  Canal  Opening.— During  the  mechan- 
ical enlargement  of  canals,  or  during  pulp  removal,  portions  of  broaches 
or  drills  may  be  broken  off  in  the  canal.  Their  removal  is  at  times 
difficult  or  practically  impossible.  If  lying  loosely  in  the  canal,  a 
probe  magnetized  by  nibbing  upon  a  steel  magnet  or  by  contact  with 
the  field  magnet  of  a  dynamo  will  remove  it.  Flagg  recommended 
a  power  magnet  attached  to  a  probe.  The  magnet  is  to  be  energized 
by  an  electric  current. 

Wrapping  a  Swiss  broach  with  cotton,  the  fibers  may  at  times  be 
made  to  engage  the  barbs  of  a  loose  broach. 

A  Donaldson  cleanser  will  also  at  times  engage  the  barbs  of  the 
broken  instrument. 

The  removing  instrument  is  passed  to  one  side  of  the  instrument  to 
be  removed  and  pressed  against  it  as  withdrawn.  The  instrument 
is  thus  gradually  jigged  out. 

Moving  the  broach  or  drill  back  and  forth  while  sulphuric  acid  or 
sodium  dioxide  solution  is  about  it  will  sometimes  loosen  it. 

If  very  deeply  placed,  common  salt  may  be  packed  over  the  broach, 
moistened,  and  sealed  in,  in  the  hope  of  rusting  it.  Tincture  of  iodine 
will  rapidly  disintegrate  steel  placed  in  it,  but  repeated  applications 
are  necessary  to  produce  the  same  effect  in  a  canal. 

Sulphuric  or  nitric  acid,  aqua  regia,  or  25  per  cent,  pyrozone  may 
be  sealed  in  to  effect  its  chemical  solution.  The  tip  of  a  fine  Donald- 
son cleanser  deeply  seated  in  the  apical  third  of  a  fine  canal  is  practi- 
cally irremovable.  If  the  root  has  given  no  previous  trouble,  strong 
and  persistent  antiseptics,  such  as  iodoform,  are  to  be  placed  over 
it  and  the  attempt  to  remove  considered  unwarrantable.  The  head 
of  a  Gates-Glidden  drill  is  to  be  saturated  with  sodium  dioxide  or 
sulphuric  acid,  and  the  attempt  is  made  to  jig  the  piece  loose;  failing 


490     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

in  this,  an  attempt  is  to  be  made  to  pass  through  the  opening  between 
the  blades,  so  that  permanently  antiseptic  materials  may  be  made  to 
go  beyond  the  drill,  in  which  case  its  presence  is  harmless. 

Dr.  W.  S.  How  has  introduced  the  split  and  threaded  cone  socket 
shown   in   Fig.  403,  which   may   be   useful   at  times.     In  use  the 


Fig.  402 


Fig.  403 


Improved  Gates-Glidden  nerve-canal  drill  for  engine  work. 

canal  is  enlarged  after  a  direct  opening  has 
been  made  to  it,  and  the  cone  is  introduced 
and  rotated. 

In  all  cases  the  forcing  of  bits  of  broaches 
into  the  apical  tissues  during  efforts  at  removal 
is  to  be  carefully  avoided.  If  it  occur,  however, 
it  will  produce  a  chronic  apical  pericementitis, 
if  not  excite  a  septic  condition.  The  cure  lies 
in  amputation  of  the  root  apex,  although  at 
times  levelling  the  broach  with  the  root  end 
through  an  external  opening  has  been  successful. 

Perforations.^A  drill  passed  through  the 
apical  foramen  enlarges  it  unduly.  The  con- 
dition simulates  an  imperfectly  completed  fora- 
men, and  is  treated  as  for  that  condition.  (See 
p.  486.) 

A  Gates-Glidden  drill  may  perforate  a  root 
near  the  apex  by  passing  through  the  wall  of 
the  canal  in  a  direct  line  with  the  canal,  while 
the  root  end  may  be  curved  (Fig.  401). 

A  finely  pointed  root  may  be  perforated 
laterally  by  the  use  of  too  large  a  drill  or  reamer. 
The  part  should  l)e  thoroughly  sterilized  and  the  hemorrhage  checked 
by  the  use  of  alum  and  thymol,*  and  a  carefully  prepared  gutta-percha 
point  is  to  be  adapted  to  the  opening,  or  thin  oxychloride  of  zinc  run 
into  it,  after  which  a  more  stiffly  mixed  portion  may  be  very  gently 


Split  and  threaded  in- 
strument for  engaging  the 
shank  of  a  Gate.s-Glidden 
drill. 


1  Prepared  by  Parke,  Davis  &  Co. 


THE  ROOT -CANAL  FILLING  491 

packed  in.  If  subsequent  trouble  arise,  amputation  or  extraction, 
perfect  root  filling,  and  replantation  may  be  resorted  to.  If  the 
perforation  be  readily  reached,  the  inner  walls  should  be  bevelled 
and  a  smooth  plaque  of  low-heat  white  gutta-percha  should  be 
adapted,  its  edges  sealed,  and  zinc  phosphate  or  oxvchloride  of  zinc 
packed  over  it  to  secure  it  in  place.  Soft  copper  amalgam  gently 
tapped  to  place  and  later  hardened  by  the  wafering  process  is  valu- 
able. In  such  cases  the  canal  apex  is  filled  as  usual.  AVith  a  difficult 
lateral  perforation  a  bit  of  sterilized  grafting  sponge  may  be  placed 
in  the  tissue  beyond  the  perforation,  and  against  this  the  gutta- 
percha or  copper  amalgam  may  be  packed.* 

Partial  Removal  of  Pulp. — The  Col^alt  method  of  pulp  treatment 
has  been  alluded  to.    Wm.  Herbst,  of  Bremen,  advanced  the  idea  that 

Fig.  404  Fig.  405 


Lateral  perforation  due  to  holding  a  bur  at  a  Herbst's   method  of    preserving 

wrong  angle  to  the  axis  of  the  root:  .1  ,  root  canal  Plilp  stumps, 

.subsequently  filled  with  gutta-percha;  li,  perfo- 
ration filled  with  a  fitted  cone  of  gutta-percha; 
C,  oxychloride  of  zinc. 

if  the  bulbous  portion  of  the  pulp  be  devitalized  by  cobalt  and  removed, 
leaving  the  root  portions,  the  latter  will  remain  vital  if  protected  after 
a  manner  described  by  him.  The  bulbous  portion  of  the  pulp  is  cut 
away  and  the  pulp  chamber  enlarged  by  means  of  large  rose  burs. 
Over  the  pulp  stumps  a  cylinder  of  tin-foil  is  laid,  and  burnished  to  fit 
the  floor  of  the  pulp  chamber  without  pres.sure  upon  the  pulp  stumps 
(Fig.  405).  Over  this  a  filling  is  placed.  Herbst  claims  that  the  j)ulp 
stumps  will  remain  vital.  Were  this  to  be  depended  upon,  it  would 
be  a  marked  saving  of  time  and  trouble  antl  would  lessen  the  chances 
of  pericementitis  subsequent  to  pulp  removal;  but  when  it  is  known 
that  the  cobalt  of  Herbst  is  metallic  arsenic,  the  ultimate  death  and 
decomposition  of  the  pulp  remnants  seem  almost  inevitable,  and  in 
fact  do  occur.    The  method  should  not  be  employed. 

'  G.  Brunton,  England,  Dental  Cosmos,   1900. 


492     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

MUMMIFICATION  OF  THE  PULP. 

Manv  experiments  have  been  performed  relative  to  leaving  in  situ 
portions  of  pulps  and  covering  them  with  substances  having  for  their 
object  the  chemical  alteration  of  the  pulp  tissue,  so  that  no  peri- 
cementitis shall  result  from  its  putrefaction.  The  first  effort  in  this 
direction  is  credited  to  Witzel  in  1874. 

Miller/  after  many  experiments  with  various  materials,  has  shown 
that  none  but  the  most  powerful  and  penetrating  antiseptics  have 
value  as  permanent  sterilizers.  These  are  the  cyanide,  bichloride, 
and  salicylate  of  mercury,  sulphate  of  copper,  and  oil  of  cinnamon. 
Orthocresol,  carbolic  acid,  trichlorphenol,  and  zinc  chloride  penetrate 
the  pulp  tissue  rapidly,  but  are  too  diffusible,  their  effects  disappearing 
in  a  few  weeks. 

He  classifies  salicylic  acid,  eugenol,  camphophdnique,  hydro- 
naphthol,  a-naphthol  and  ^-naphthol,  aceticotartrate  of  aluminum, 
and  some  essential  oils,  resorcin,  thallin,  sulphocarbolate  of  zinc,  etc., 
as  being  of  doubtful  value. 

Those  nearly  or  quite  worthless  are  iodoform,  basic  anilin  coloring 
matters,  borax,  boric  acid,  dermatol,  europhen,  calcium  chloride, 
hydrogen  dioxide,  sozoiodol  salts,  tincture  of  iodine,  spirit  of  camphor, 
and  naphthalin. 

The  preparation  giving  the  best  results  consisted  of  mercuric 
chloride,  0.0075  gram;  thymol,  0.0075  gram,  in  tablet  form. 

The  pulp  is  devitalized;  the  crown  portion  and  all  the  root  portion 
readily  accessible  are  removed;  one  of  the  tablets  is  placed  in  the  pulp 
chamber,  crushed  by  means  of  an  amalgam  plugger,  and  covered  with 
gold-foil.  The  mercury  salt  tends  to  discolor  the  crown  of  the  tooth, 
so  that  its  employment  should  be  restricted  to  the  posterior  teeth; 
indeed,  the  necessity  for  its  use  would  be,  as  a  rule,  found  with  these 
teeth,  being  those  from  which  it  is  most  difficult  to  extract  pulp 
remnants.  Miller  expresses  faith  in  the  power  of  oil  of  cinnamon  to 
permanently  sterilize  pulp  fragments. 

Soderberg^  recommended  a  paste  composed  as  follows: 

"Sf. — Alum  exsic, 
Thymol. 

Glycerol iia,     oJ- 

Zinci  oxidi q.  s.  to  make  a  stiff  paste.— M. 

I  Proceedings  of  Columbian  Dental  Congress,  1893. 
''  Dental  Cosmos,  November,  1895. 


MUMMIFICATION  OF  THE  PULP  493 

It  is  preferable  to  add  the  zinc  oxide  as  needed  or  to  make  a  small 
quantity  of  the  paste  frequently,  as  it  gradually  hardens.  To  the 
paste  used  a  crystal  of  cocaine  is  added  to  prevent  pain.  Bennette,  of 
England,  has  advised  the  use  of  paraform  incorporated  in  the  paste,  for 
its  well-known  antiseptic  and  hardening  effects.  Greenbaum  sug- 
gested the  use  of  a  drop  of  40  per  cent,  formaldehyde  solution  to  be 
incorporated  with  the  paste.  Both  reduce  the  pulp  to  the  consistence 
of  catgut. 

Soderberg  reopened  cases  months  after  application  of  the  paste  to 
pulp  stumps,  and  found  them  shnmken  and  with  an  odor  of  thymol 
about  them. 

He  applied  the  paste  in  the  manner  shown  in  Figs.  406  and  407. 
In  1900  Soderberg^  reported  the  use  of  the  paste  in  about  nine  hundred 
cases,^  of  which  two  hundred  and  twenty  were  test  cases  of  from  two 

Fig.  406  Fig.  407 


a,  caries  exposing  a  horn  of  the  pulp.  a,  root  portion  of  pulp;  b,  mummifyini!  paste; 

c,  zinc  phosphate;  d,  gold  or  amalgam. 

to  six  years'  standing.  He  claims  that  in  no  case  did  aj)ical  peri- 
cemental disturbance  arise  from  the  use  of  the  paste  as  described. 

This  method  has  met  with  much  opposition  from  prominent  oper- 
ators, who  prefer  the  thorough  cleansing  and  filling  of  the  canals. 
No  doubt  the  rational  method  of  procedure  is  to  cleanse  the  canals 
as  well  as  possible,  and  to  use  the  paste  against  unremovable  pulj) 
stumps. 

The  best  results  were  obtained  when  arsenic  was  applied  for  a 
limited  time  only  in  order  that  the  arsenic  should  not  penetrate  too 
deeply.    In  view  of  Kirk's  observations  (p.  480)  this  would  seem  wise. 

While  the  paste  may  effect  mummification  of  entire  canal  filaments 
of  pulp,  leakage  is  always  imminent  about  .shninken  pulps,  and  the 
only  safeguard  is  the  antiseptic  effect  of  the  paste.       This  is  much 

'  Dental  Cosmos.  s  Items  of  Interest,  1898. 


494     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

enhanced  if  the  bulk  of  putrefiable  material  be  replaced  with  the  anti- 
septic paste  used  as  a  root  filling.  Many  such  root  fillings  have  done 
good  service  for  many  years. 

A  certain  percentage  of  failures  would  be  no  argument  against  the 
employment  of  the  method  when  indicated,  as  no  method  is  infallible 
in  all  circumstances,  and  particularly  in  those  in  which  the  method 
is  indicated. 

DIGESTION  OF  THE  PULP. 

Harlan  has  recommended  the  digestion  of  inaccessible  pulp  rem- 
nants with  a  vegetable  ferment.  The  pulp  chamber  is  dried  and  then 
moistened  with  a  1  to  300  solution  of  hydrochloric  acid  and  packed 
with  a  paste  composed  as  follows : 

I^. — Papain  gr.  v 

Price's  pure  glycerin ITliv 

"2  oT  hydrochloric  acid lllv. 

Over  this  is  placed  a  layer  of  blotting  paper  soaked  in  liquid  vaseline. 
The  cavity  is  sealed  with  oxyphosphate  of  zinc  or  oxysulphate  of  zinc. 

The  paste  should  be  freshly  made  in  the  above  proportions,  reduced 
to  suit  the  quantity  needed.  The  application  requires  a  few  days 
to  reduce  the  pulp  tissue  to  a  jelly-like  digested  mass,  which  can 
readily  be  washed  away.  It  is  recommended  that  the  papain  be  kept 
in  a  dark-glass  bottle.  It  is  harmless  to  living  tissue  which  is  not 
digested.  Alcohols,  tannin,  lead,  mercuric  chloride,  nitric  acid,  and 
salts  of  heavy  metals  are  incompatibles. 

Such  pulp  digestion  is  only  a  preliminary  to  root  filling. 


CHAPTER    XVIII. 
GANGRENE  OF  THE   PULP. 

Definition. — By  gangrene  of  the  pulp  is  meant  its  death  through  an 
interference  with  its  nutrition.  It  may  be  partial,  as  when  an  abscess 
in  the  pulp  or  violent  irritation  causes  the  bulbar  portion  to  die,  the 
canal  portions  being  found  alive;  or  when  only  one  canal  portion  is 
dead,  the  others  being  alive.    Either  dry  or  moist  gangrene  may  occur. 

Causes. — It  is  probable  that  a  construction  of  apical  root  tissue 
(hypercementosis)  about  the  pulp  may  so  constrict  it  as  to  bring  about 
its  death.  Sudden  shocks,  such  as  occur  from  thread,  string,  or  cigar 
biting,  or  blows  or  rapid  movement  in  regulating  or  wedging,  or  non- 
fixation  after  regulation,  may  cause  torsion  or  tension  of  the  blood- 
vessels entering  the  apex  of  the  pulp. 

These  influences  may  either  cause  pulp  hyperemia  or  strangulation 
of  the  apical  bloodvessels,  or,  possibly,  an  area  of  apical  thrombosis, 
cutting  off  the  nutritive  supply  to  the  pulp.  Septic  or  aseptic  inflam- 
mation of  the  pulp  may  cause  its  total  death.  Death  of  pulp  tissue 
due  to  arsenic  produces  residts  in  nowise  differing  from  gangrene, 
provided  the  pulp  be  left  in  situ.     (See  p.  83.) 


DRY  GANGRENE  OF  THE  PULP. 

Definition. — By  dry  gangrene  of  the  dental  pulp  is  meant  its  death 
in  toto  and  its  subsequent  transformation  into  a  dry,  shrivelled  mass 
occupying  the  pulp  chaml)er  and  canal. 

Causes  and  Pathology. — If  the  pidp  die  and  remain  under  conditions 
which  exclude  bacteria  from  contact  with  it,  the  water  of  the  pulp 
may  be  removed,  leaving  the  organ  as  a  tough,  shrivelled  mass  (Fig. 
408).  The  conditions  most  favorable  seem  to  be:  (1)  ])ulp  death 
from  some  aseptic  cause;  (2)  constriction  of  the  apical  foramen; 
(3)  the  presence  of  secondary  dentine  over  the  bulbar  portion  of  the 
pulp;  (4)  the  capping  of  the  pulp  with  zinc  oxychloride  or  formagen 
paste;  (5)  the  covering  of  pulp  stumps  with  a  paste  containing  a  tanni- 
fying  substance,  such  as  alum,  formaldehyde,  or  tannin. 


496  GANGRENE  OF  THE  PULP 

The  water  necessary  to  putrefaction  is  abstracted,  either  naturally 
or  chemically,  and  probably  bacteria  are  at  the  same  time  excluded, 
either  mechanically  or  because  the  chemical  substances  used  have 
penetrated  the  pulp  tissue,  acting  as  antiseptics. 

Symptoms. — ^The  tooth  has  a  nearly  normal  color,  but  under  reflected 
light  is  seen  to  have  lost  perfect  translucency.  There  is  no  response 
to  thermal  or  electric  tests  for  pulp  vitality.  The  dentine  is  insen- 
sitive to  cutting  instruments,  and  the  cuttings  upon  the  bur  have  no 
odor.  There  is  no  odor  or  fluid  in  the  pulp  canal  when  this  is  entered, 
and  the  pulp  is  found  as  a  tough,  dry  mass  not  unlike  that  seen  in 
a  dry  extracted  tooth  which  contained  a  vital  pulp  at  the  time  of 
extraction.     These  cases  are  relatively  rare. 

Tests  for  Pulp  Vitality. — The  diagnosis  of  pulp  vitality  or  death 
being  in  practice  almost  daily  required,  the  decisive  tests  are  here 
indicated. 

A  tooth  containing  a  vital  pulp  is  translucent;  that  containing  a 
dead  one  always  opaque  to  transmitted  light. 

An  electric  mouth  lamp  with  a  mirror  so  arranged  as  to  reflect  the 
light  upon  the  lingual  surface  of  the  tooth  will  supply  the  means  for 
this  test.  In  its  absence  strong  sunlight  may  be  reflected  by  means  of  a 
mouth  mirror,  but  is  not  nearly  so  good  a  means  as  the  electric  light 
(Fig.  326). 

If  the  tooth  be  isolated  by  means  of  rubber  dam  and,  first,  cold  water 
be  thrown,  or,  later,  ethyl  or  methyl  chloride  be  sprayed  upon  it  or  upon 
the  filling  contained  in  it,  absence  of  response  will  indicate  either  pulp 
death  or  the  formation  of  a  quantity  of  secondary  dentine.  In  the 
latter  case  the  test  must  be  renewed  as  the  excavation  proceeds. 

A  hot  burnisher  or  hot  gutta-percha  applied  to  a  filling  or  dentine,  or 
very  hot  water  thrown  upon  an  isolated  tooth,  should  provoke  at  least 
a  delayed  response  from  a  vital  pulp. 

Woodward  has  shown  that  if  a  few  cells  of  a  cataphoric  apparatus 
are  in  action  and  the  positive  electrode  be  applied  to  the  dentine  or 
metal  filling  in  a  vital  tooth,  while  the  negative  pole  is  at  the  cheek 
or  wrist  of  the  patient,  a  distinct  sensation  should  be  felt,  while  in 
case  of  a  dead  pulp  there  will  be  no  response;  usually  even  a  small  fill- 
ing will  transmit  a  distinct  shock  in  a  vital  tooth  which  is  absent  in  a 
devitalized  tooth.  A  mild  interrupted  current  has  also  been  used  for 
the  test.  There  may  be  no  response  through  a  metal  filling,  while 
such  response  may  be  obtained  by  packing  wet  cotton  against 
the  dentine  after  some  drilling.     A  mild  current  should  always  be 


DRY  GANGRENE  OF  THE  PULP 


497 


used  unless  there  is  no  response,  when  the  strength  of  the  cu  rrent  should 
be  increased.  If  the  filling  reach  the  gum,  the  current  may  be  transmit- 
ted by  it.  The  possibility  of  contact  of  the  filling  with  another  in  a  vital 
tooth  is  to  be  remembered.     Insulation  with  rubber  dam  is  indicated. 

In  doubtful  cases,  such  as  that  shown  in  Fig.  410,  the  a:-ray  skia- 
graph is  valuable,  and  indicates  at  least  the  removal  of  the  filling  for 
further  diagnosis  and  treatment.  When  dentine  is  insensitive,  pulp 
death  shoidd  be  suspected. 

A  strong  odor  of  putrefaction  may  be  o})tained  from  bur  cuttings 
in  cases  of  moist  gangrene  only.  This  must  be  dift'erentiated  from 
the  odor  of  decayed  dentine,  which  usually  also  has  an  acid  character. 
In  case  of  partial  death  of   the  pulp   not  discoverable  by  the  tests 


Fig.  408 


Fig.  409 


Fig.  410 


Dry  gangrene  of  the 
pulp:  PA'',  pulp  nodule; 
DP,  .'ihrivelled  pulp. 
(From  a  specimen  of 
pulp  extracted  intact 
in    this   condition.) 


Caries;  moi.st  gangrene  in  impris- 
oned temporary  molar.  (Skiagraph 
by  Hagopian  from  editor's  case.) 


Skiagrapli  of  unfilled 
root  canals  with  large 
mass  of  filling  material 
built  in  over  thero. 
(Price.') 


given  above,  a  fine,  sharp  probe  passed  into  contact  with  the  pulp 
remnant  will  demonstrate  its  vitality. 

Treatment. — If  septic  matter  be  introduced  a  violent  pericementitis 
may  be  lighted  up;  but  if  aseptic  precautions  be  employed  in  opening 
the  canal,  and  this  be  kept  under  the  influence  of  a  germicide,  such  as 
5  per  cent,  formaldehyde  or  sodium  dioxide,  the  root  may  be  filled  by 
the  immediate  method — i.  e.,  when  opened  and  sterilized  it  is  to  be 
dried  and  then  moistened  with  eucalyptol  and  the  excess  of  this 
removed;  previously  prepared  cones  of  temporary  stopping  are  then 
packed  into  the  root  or  another  root  filling  employed.  The  method 
of  moistening  the  canal  with  forma-percha  and  then  placing  the  cones, 
or  the  use  of  cotton,  silk,  or  asbestos  fibers  saturated  with  forma- 
percha  (see  p.  488),  has  all  the  advantages  of  the  temporary  antiseptic 
filling,  with  the  added  merit  of  permanency  if  the  indications  declare 
a  success. 

>  Items  of  Interest,  1901. 

32 


498  GANGRENE  OF  THE  PULP 

A  temporary  filling  of  pink  base-plate  gutta-percha  is  to  be  inserted 
in  the  crown  cavity  until  all  irritation,  if  any,  subsides. 

Slight  aseptic  apical  irritation  may  be  anticipated  as  a  matter  of 
precaution  by  the  use  of  iodine  as  a  counterirritant  at  the  time  of  root 
filling.  (See  p.  428.)  Such  irritation  is  either  mechanical  or  due  to 
the  chemical  substances  used. 


MOIST  GANGRENE  OF  THE  PULP. 

Definition. — By  moist  gangrene  of  the  pulp  is  meant  death  of  pulp 
tissue  en  masse  and  its  subsequent  decomposition  by  the  action  of 
putrefactive  agencies.  As  putrefactive  decomposition  is  the  essential 
feature  in  these  cases,  and  that  which  gives  the  process  its  pathological 
significance,  the  causes,  nature,  effects,  and  treatment  of  putrefactive 
decomposition  of  the  pulp  are  included  under  this  subheading  (p.  83), 

Causes. — The  causes  of  moist  gangrene  are  such  as  may  cause  the 
death  of  the  pulp  and  its  subsequent  decomposition  by  bacteria. 
Without  bacteria  putrefaction  cannot  occur.  Among  these  the 
Bacillus  gangrense  pulpse  (Arkovy)  figures  prominently.^  Four  types 
of  cases  are  seen:  (1)  In  teeth  apparently  sound;  (2)  in  teeth  filled, 
but  the  canals  not  treated — i.  e.,  death  of  the  pulp  has  occurred  after 
filling;  (3)  in  teeth  filled  with  canals  partly  filled;  (4)  in  teeth  having 
open  cavities  and  canals. 

In  the  first  type  of  cases  the  bacteria  may  enter  by  way  of  the  blood 
channels,  but  it  is  not  improbable  that  slight  cracks  or  histological 
defects  in  the  enamel  may  admit  to  the  dentinal  tubules  the  necessary 
bacteria,  or  that  they  may  gain  entrance  by  way  of  the  cementum  and 
dentine  at  the  neck  of  the  tooth.    (See  Caush's  tubes.) 

A  case  presenting  some  analogy  to  these  teeth  is  that  of  an  egg  with 
apparently  perfect  shell,  but  in  which  intense  decomposition  has 
occurred.  That  the  gases  and  other  odorous  products  are  somewhat 
confined  the  author  proved  to  his  dismay  as  a  boy  by  smashing  with  a 
hatchet  one  found  in  the  brush. 

Many  of  these  teeth  do  not  develop  abscesses  even  after  the  tooth 
has  become  dark  in  color.  If  the  dentine  be  exposed  as  at  the  incisal 
edge,  the  abscess  may  develop. 

In  the  filled  cases  crevices  about  crown  and  root  fillings  may  admit 
bacteria,  which  may  pass  through  the  tubules  of  even  secondary 

'  Siberth  and  Goadby  regard  tliis  microorganism  as  a  variety  of  Bacillus  mesentericus,  prob- 
ably "niger."     Mycology  of  the  Mouth,  p.  148. 


MOIST  GANGRENE  OF  THE  PULP 


499 


Pigment. 


Fig.  411 
Sulphur  +  hemoglobin. 


dentine  in  .some  amount.  On  the  other  hand,  it  i.s  irrational  not  to 
admit  the  po.s.sibiUtv'  of  an  infection  via  the  circulation. 

In  cases  of  obvious  pulp  infection  beneath  fillings — e.  g.,  .suppura- 
tion of  the  pulp — the  bacteria  necessary  are  in  situ. 

In  the  open  ca.ses  the  infection  obviously  arises  from  the  mouth. 

Pathology  and  Morbid  Anatomy. — ^The  pulp  being  wholly  or  partly 
dead  from  any  cause  whatever,  saprophytic  bacteria  gain  access  to 
it,  and  the  serial  decomposition  it 
undergoes  is  in  exact  correspondence 
with  that  of  moist  gangrene  or  putre- 
faction in  other  localities. 

In  this  serial  decomposition  albu- 
minous substances  are  first  trans- 
formed into  peptones  and  allied 
sul)stances,  .some  of  them  being  very 
toxic.  Compound  ammonias,  known 
as  ptomains,  or  animal  alkaloids, 
such  as  putrescine,  neuridine,  and 
cadaverine,  are  probably  next  formed. 
Next  the  nitrogenous  bases — leucin, 
tyrosin  (amido-acid),  and  the  amines 
(methyl,  ethyl,  and  propyl) — make 
their  appearance,  together  with  or- 
ganic fatty  acids.  Next  aromatic 
products,  indol,  phenol,  cresol,  etc., 
and  finally,  hydrogen  sulphide, 
ammonia  sulphide,  carbon  dioxide, 
and  water.  By  alternating  proces.ses 
of  hydration,  reduction,  and  oxida- 
tion, bodies  of  increasing  simplicity 
of  chemical  composition  are  formed.^ 
The  contents  of  the  tubule  (fibrillae) 

also  are  putrefied.  The.se  products  are  derived  from  the  following 
chemical  constituents  found  in  normal  pulps,  according  to  Hodgen : 
Proteins  and  albuminoid,  fibrin,  hemoglobin,  collagen,  elastin,  fats, 
tripalmitin,  stearin,  and  olein. 

The  irritant  bodies  are  probably  the  gases  and  the  ptomains  which 
have  experimentally  been  found  capable  of  producing  suppuration  in 
the  absence  of  bacteria. 


H.,0  and  H3S 

Aromatic  and 
fatty  prod- 
ucts. 

Ptomaine. 


Peptones. 


Diagram  illustrating  the  more  complete 
decomposition  of  the  pulp  at  its  coronal 
end. 


'  Ziegler,  General  Pathology. 


500 


GAXGRENE  OF  THE  PULP 


IMiller^  found,  in  the  deepest  portions  of  the  degenerating,  putrefying 
pulps,  where  inflammation  and  suppuration  were  in  progress,  a  pre- 
ponderance of  small  cocci  and  diplococci,  and  proceeding  toward  the 


Fig.  412 


Fig.  413 


Fig.  414 


..V 


Fig.  415 


£^3         <vaa^ 


Fig.  417 


'.%Uk. 


i'ili 


Fig.  418 


.^  •  ""t^ 


r        /» 


Fig.  419 


1''  /   '^ 


.    / 


open  pulp  chamber  an  increasing  number  of  large  cocci,  several  forms 
of  bacilli,  vibrios,  and  other  spirilla;,  spirochetse,  and  long  thread 
forms  (Figs.  412  to  419).    Figs.  418  and  419  are  from  the  same  pulp; 


'  Dental  Cosmoe,  1894. 


MOIST  GANGRENE  OF  THE  PULP  501 

Fig.  415  was  taken  from  the  radicular  portion  of  a  pulp  which  was 
alive  and  suppurating;  Fig.  412  was  from  the  putrid  crown  portion. 
Miller  found  that  bacteria  of  pulp  putrefaction  cultivated  in  gelatin, 
with  and  without  the  access  of  air,  exhibited  a  difference  in  the  poison- 
ous properties  of  their  products.  Those  developed  with  free  access  of 
air  produced  stronger  reaction,  and  more  extensive  suppuration  than 
those  developed  without  the  access  of  air. 

Arkovy,^  in  an  examination  of  43  cases  of  chronic  apical  abscess, 
pulp  gangrene,  etc.,  found  the  Bacillus  gangrense  pulpa^  present  in  41 ; 
the  Staphylococcus  pyogenes  aureus  in  15;  Staphylococcus  pyogenes 
albus  in  8;  Staphylococcus  pyogenes  citreus  in  2;  Streptococcus 
pyogenes  in  10,  and  Bacillus  pyocyaneus  in  4. 

He  found  the  Bacillus  gangrenae  pulpae  in  mouths  free  of  caries  as 
well  as  in  mouths  containing  carious  teeth,  and  established  the  fact 
that  it  is  pleomorphous  (bacillus  and  coccus  form). 

He  inoculated  iiealthy  pulps  with  this  })acterium,and  found  that  in 
pure  culture  it  produced  total  gangrene  without  suppuration;  while 
mixed  cultures,  and  even  the  mixed  pleomorphic  forms  of  the  same 
bacillus,  produced  chronic  pulpitis. 

On  gelatin  cultures  a  putrid,  cheese-like  odor  was  perceptible.  The 
germ  is  subject  to  the  antiseptic  effects  of  strong  acids,  alkalies,  carbolic 
acid,  and  tincture  of  iodine,  which  explains,  in  part,  the  success  of 
the  treatment  hereinafter  mentioned. 

Arkovy's  demonstration  seems  a  satisfactory  explanation  of  cases 
of  quiet  death  of  pulps  under  fillings. 

The  hydrogen  sulphide  combines  with  NH^  to  form  ammonium 
sulphide  (NHJjS,  which,  again,  combines  with  the  iron  in  the  hemo- 
globin of  the  red  blood  corpuscles,  producing  ferrous  sulphide,  which, 
entering  the  tubules,  stains  the  dentine  a  slaty-gray  or  bluish  black 
color.  Other  derivatives  of  hemoglobin  may  be  responsible  for  the 
yellowish  brown  discoloration  often  seen  in  cases  in  which  bacteria 
have  not  reached  the  pulp  until  long  after  pulp  death.  The  color 
is,  therefore,  not  due  to  the  presence  of  hydrogen  sulphide. 

Fig,  411  is  a  diagram  illustrating  these  changes;  it  being  assumed 
that  the  decomposition  is  most  advanced  at  the  crown  portion  of  the 
pulp,  owing  to  the  entrance  of  bacteria  at  that  point. 

In  the  early  stage  of  the  process  the  gangrenous  pulp  resembles 
a  yellowish  mass  of  sloughing  tissue,  which  can  be  easily  removed. 
In  the  later  stages  it  is  more  decomposetl  and  dark,  and  vields  to  the 

•  Synopsis  by  Suderherg,  Dental  Cosmos,  1899. 


502  GANGRENE  OF  THE  PULP 

broach.  In  the  final  stages  nothing  but  fluid,  or  even  an  ahiiost  dry 
canal,  may  be  found.  This  last  condition  must  not  be  confounded 
with  dry  gangrene.  If  fluid,  or  odor  without  fluid,  be  present  the  case 
is  one  of  moist  gangrene. 

Symptoms. — ^As  a  rule,  the  tooth  presents  at  least  an  opacity  upon 
transmission  of  light,  but  usually  has  the  bluish  or  brownish  discolor- 
ation mentioned,  most  marked  at  the  cervical  third  of  the  crown  and 
most  noticeably  upon  the  lingual  side.  There  is  an  absence  of  response 
to  thermal  and  electric  tests.  Occasionally  the  patient  complains  of 
a  bad  taste  in  the  region  of  the  tooth.  This  is  due  to  slow  leakage. 
The  symptoms  of  septic  apical  pericementitis  may  be  localized  about 
the  apex  of  the  tooth,  or  at  times  the  pain  of  incipient  pericementitis 
may  be  reflected  or  a  history  of  apical  abscess  may  be  obtained,  con- 
firmed by  the  presence  of  a  fistula.  Occasionally  the  patient  complains 
of  apical  pain  upon  passing  from  a  warm  to  a  cold  atmosphere  and 
vice  versa.  Upon  drilling  out  a  filling  the  odor  of  putrefaction  may 
be  clearly  noticed,  even  before  the  entrance  of  the  canal.  The  odor 
of  the  bur  cuttings  is  diagnostic  in  less  pronounced  cases.  The  mal- 
odorous gases  may  be  present  in  quantity  without  acute  symptoms  of 
pericementitis. 

It  is  presumptive  that  in  some  cases  these  gases  gradually  escape 
through  the  tubules  and  by  way  of  leaks  about  the  fillings,  a  fact 
which  may  act  favorably  by  preventing  accumulation  and  the  forma- 
tion of  an  apical  abscess. 

A  confusing  condition  clinically  is  found  where  one-half  of  a  pulp 
has  died  and  undergone  decomposition,  as  in  molars,  the  other  half 
remaining  vital,  although  the  seat  of  infection  and  inflammatory 
action.  So  far  may  this  condition  go,  that  abscess,  acute  or  chronic, 
may  be  present  upon  the  root  of  one  tooth  long  before  the  second 
segment  of  the  pulp  has  succumbed.  The  diagnosis  of  such  cases  is 
made  l)y  the  light  test,  by  obtaining  the  painful  reaction  to  heat  and 
perhaps  to  electricity,  and  usually  some  tenderness  upon  percussion 
upon  some  particular  portion  of  the  tooth;  upon  opening  the  tooth 
the  peculiar  condition  described  is  found.  The  a;-ray  should  show  the 
condition. 

In  one  case  of  a  lower  molar  with  a  fistula  related  with  the  distal 
root  1  f(Mind  the  jMilp  apparently  vital  upon  entering  the  pulp  chamber 
with  a  l)ur  at  a  point  al)out  midway  between  the  horns.  There  was 
apparently  a  persistence  or  hypertrophy  of  the  ]>ulp  bulb  attached  to 
the  mesial  filaments.    The  distal  canal  was  found  to  contain  only  the 


MOIST  GANGRENE  OF  THE  PULP  503 

fluid  remains  of  a  dead  pulp  filament.  In  cases  seen  at  the  right 
time  the  bulbal  half  of  a  pulp  may  he  gangrenous  without  positive 
putrefaction,  while  the  apical  half  is  still  vital. 

J.  H.  McQuillen^  recorded  a  case  of  longitudinal  fracture  of  a 
bicuspid  tooth  extending  from  the  sulcus  to  the  bifurcation  of  the 
roots,  and  which  was  apparently  due  to  the  expansion  of  the  gases 
of  decomposition.  Poinsot^  records  a  similar  case,  and  states  that 
several  teeth  containing  decomposed  pulps  confined  in  a  glass  tube 
caused  the  latter  to  break. 

Observations  previous  to  that  of  McQuillen  have  recorded  a  sound, 
as  of  an  explosion,  to  have  occurred  simultaneously  with  the  fracture 
of  the  tooth.  I  have  looked  all  my  professional  life  for  such  a  case, 
but  have  never  been  able  to  eliminate  the  possibility  of  fracture  from 
ordinary  causes. 

Treatment. — The  general  principle  of  treatment,  in  all  cases  present- 
ing without  symptoms  of  apical  pericementitis,  is  the  disinfection  of 
canals,  the  removal  of  all  decomposed  and  decomposing  pulp  tissue, 
prevention  of  infection  of  the  pericementum,  and  hermetical  sealing 
of  the  apex  and  body  of  the  canal  by  means  of  appropriate  root  fillings. 

In  all  cases  the  imminent  danger  and  that  to  be  guarded  against  is 
to  avoid  mechanically  carrying  a  portion  ever  so  minute  of  infective 
material  past  the  apical  foramen.  This  implies  either  great  dexterity, 
or  the  use  of  a  germicide  which  shall  sterilize  the  pulp  tissue  l)efore 
the  attempt  is  made  to  remove  it.  Should  any  pass  through,  it  must 
be  sterilized  l)y  strong  germicides  passed  after  it. 

Probably  the  safest  plan  to  follow,  except  in  emergencies,  is  to  care- 
fully sterilize  the  mouth  with  a  1  to  2000  solution  of  mercuric  chloride 
in  hydrogen  dioxide,  or  a  solution  of  potassium  permanganate,  or  to 
place  the  rubber  dam  and  sterilize  the  crown  and  cavity. 

The  tooth  is  then  to  be  carefully  opened  until  the  pulp  chamber  is 
freely  exposed. 

Into  this  is  then  placed  a  pellet  of  cotton  saturated  with  a  10  or  20 
per  cent,  solution  of  formalin;  or  geranium-formoP;  or  tricresol  and 
formalin,  etjual  parts  (Buckley).  The  tooth  is  then  sealed  with 
adhesive  cement  or  hot  temporary  stopping  or  soft  amalgam  foi 
twenty-four   or   forty-eight    hours.      The    editor    often    makes    the 

'  Dental  Cosmos,  1871.  =  Ujiii..  1901. 

'  (leraiiiuin-forraol  introduced  by  .Andre  and  de  .Marion,  I'Odoiilologie;  abs^traot  by  Inter- 
national Dental  .Journal,  1901: 

I^. — Formaldehyde 40  part>. 

lOssence  of  geranium  di.stilled 20  parts. 

Alcohol  80° 40  parts. 


504  GANGRENE  OF  THE  PULP 

temporary  covering  used  for  arsenic  (p.  477),  or  even  uses  the 
permanent  amalgam  in  the  same  way,  adding  to  it  when  the  treat- 
ment is  completed. 

According  to  Buckley  the  formalin  unites  with  the  ammonia  to  form 
urotropin  and  with  hydrogen  sulphide  to  form  methyl  alcohol  and 
sulphur.  The  tricresol  is  supposed  to  act  upon  the  fatty  compounds, 
changing  them  into  a  compound  resembling  lysol.  Thus,  antiseptic 
substances  are  formed  from  poisonous  ones.  A  portion  of  the  solid  or 
polymerized  form  of  formaldehyde  may  be  introduced  into  the  moist 
pulp  chamber,  and  has  an  analogous  action. 

At  a  subsequent  sitting  the  canals  are  thoroughly  opened  under 
rubber  dam  and  cleansed  under  antiseptic  precautions,  one  of  the 
best  being  a  5  per  cent,  aqueous  solution  of  formalin,  or,  if  preferred, 
the  tricresol  and  formalin  may  be  used. 

The  pulp  having  been  mechanically  removed  and  the  canals  enlarged 
(see  p.  482),  the  canals  are  thoroughly  dried  with  hot  air  and  a 
dressing  of  5  per  cent,  formalin  or  geranium-formol  or  tricresol  2  parts, 
formalin  1  part  (Buckley)  should  be  sealed  in  it  for  about  three  days, 
when,  as  a  rule,  all  odor  will  be  gone  and  the  canal  may  be  filled.  In 
drying  with  the  compressed-air  syringe,  care  should  be  employed  to 
avoid  extensive  emphysema  of  the  cheek,  which  may  be  induced  by 
intense  pressure.  If  it  occur,  the  emphysema  should  be  reduced  by 
manipulation,  with  a  view  to  gently  forcing  the  air  back  through  the 
root.    Christensen^  and  L.  Greenbaum  have  each  reported  a  case. 

By  these  means  all  parts  of  the  dead  pulp  are  sterilized,  and  if  any 
inaccessible  portion  of  root  canal  remain  it  should  be  treated  according 
to  Rhein's  method  of  placing  a  zinc  probe  in  the  canal,  which  should 
be  filled  with  a  solution  of  mercuric  chloride  in  hydrogen  dioxide 
(1  to  500).  The  positive  pole  of  the  cataphoric  current  should  be 
applied  to  the  probe,  with  the  moist  negative  sponge  electrode  at  the 
cheek.  From  three  to  seven  minutes  with  a  force  of  from  1  to  5  mi. 
of  current  are  required  to  form  oxychloride  of  zinc  which  occupies 
the  inaccessible  portion  of  the  canal.  ^     (See  p.  485.) 

In  the  absence  of  the  cataphoric  current,  or  even  after  its  use,  the 
paraform  alum  paste  given  on  p.  488  should  be  packed  into  the 
apical  portion  of  the  root  as  a  persistently  germicidal  canal  occupant; 
as  even  long-established  fistulae  have  been  cured  in  this  manner  it  is 
a  rational  means  of  treatment. 

If  exigencies  demand  it,  root  sterilization  may  be  immediately 

'  Dental  Cosmos,  1904,  p.  151.  ''■   Ibid.,  1905,  p.  1190. 


MOIST  GANGRENE  OF  THE  PULP  505 

attempted  after  the  rubber  dam  has  been  placed  and  the  crown 
washed  with  5  per  cent,  formalin  or  alcohol  and  water. 

A  little  dry  sodium  dioxide  is  placed  upon  a  slab  with  a  drop  of 
water  near  it. 

A  broach  is  drawn  through  the  water,  then  through  the  powder, 
and  the  adherent  powder  carried  to  the  canal  and  gently  passed  into 
the  moist  putrid  contents  of  the  canal;  a  reaction  occurs  between  the 
water  and  sodium  dioxide  as  follows  ^2L^^-\-2Y{fi^Y{^^  +  2KaiO\{, 
producing  hydrogen  dioxide  and  sodium  hydrate. 

The  sodium  hydrate  or  lye  saponifies  all  fatty  matters  and 
destroys  organic  matter,  even  living  matter,  and  the  hydrogen  dioxide 
liberates  nascent  oxygen,  which  is  a  disinfectant. 

The  result  of  the  reaction  should  be  washed  out  with  a  gentle  stream 
of  warm  water,  while  a  broach  is  gently  passed  to  and  fro  through  the 
mass.    The  action  is  then  repeated  as  far  as  it  can  be  carried. 

The  danger  in  the  use  of  this  material  lies  in  the  possibility  of  the  pro- 
duction of  a  chemical  inflammation  of  the  apical  tissue  if  tiie  foramen 
be  open,  which  inflammation  may  be  severe,  or  in  the  possibility  of  a 
non-sterilization  of  the  contents  of  inaccessible  canals.  For  this 
reason  it  may  be  well  to  use  a  5  per  cent,  formalin  solution  for  the 
purpose  of  completing  the  sterilization  in  the  more  open  roots,  and 
20  per  cent,  formalin  or  25  per  cent,  ethereal  pyrozone  (H^O^)  for  the 
finer  roots. 

Following  this  the  root  filling  is  either  attempted  immediately  with 
removable  antiseptic  root  fillings  or  a  dressing  of  5  per  cent,  formalin 
introduced  into  the  dried  canal  for  a  few  days. 

Any  irritation  of  chemical  nature  may  be  treated  in  anticipation  iiy 
the  use  of  counterirritants  applied  to  the  gum. 

The  filling  of  canals  by  driving  wood  points  saturateil  in  carbolic 
acid  into  the  infected  canals,  forcing  carbolic  acid  by  pressure  into 
the  apical  tissue,  and  the  filling  with  gutta-percha  are  all  successful 
in  many  cases,  but  there  is  much  likelihood  of  apical  abscess,  or,  at 
least,  of  traumatic  or  chemical  irritation,  which  it  requires  much 
courage  not  to  undo,  with  a  patient  complaining,  and  some  doubt  as 
to  whether  an  abscess  will  result,  so  that  more  gradual  yet  thorough 
work  is  advisable,  at  least  for  the  young  practitioner  who  nuist 
retain  the  confidence  of  the  patient. 

Hoffendahl,'  of  Berlin,  has  extended  the  tlemonstration  of  Zierlerand 
shown  that  the  constant  galvanic  electric  current  from  a  battery  of 

>  Dental  Cosmos,  1905. 


506  GANGRENE  OF  THE  PULP 

from  30  to  40  Leclanche  cells  to  overcome  the  resistance  of  the  tissues 
will  electrolyticallj  decompose  0.75  per  cent,  sodium  chloride  solution 
and  drive  nascent  chlorine,  H^O^,  and  oxygen  through  even  fine  root 
canals  and  into  the  infected  tissue  about  an  abscess  cavity.  Thus, 
electrolysis  and  cataphoresis  are  brought  into  play.  The  current  does 
not  pass  through  the  side  of  the  root;  a  street  or  central  direct  current 
with  a  rheostat  attachment  reducing  the  current  to  from  0  to  80 
volts  is  equally  effective. 

The  tooth  should  be  rubber  dammed  to  insulate  the  gum.  The 
canal  should  be  carefully  cleansed,  so  as  not  to  permit  ptomains  to 
pass  into  the  apical  tissues,  and  then  filled  with  a  sodium  chloride 
solution.  A  fine  platinum  electrode  is  introduced  into  the  moist  canal, 
and  must  be  attached  to  the  positive  pole  of  the  battery.  A  large 
moist  negative  electrode  is  to  be  applied  to  the  hand  to  lessen  resistance 
and  conduct  the  current  to  the  negative  pole  of  the  battery.  The  size 
prevents  uncomfortable  sensations  about  the  tooth.  The  rheostat 
should  be  manipulated  so  as  to  introduce  the  current  gradually  until 
about  1.5  mi.  is  recorded  on  the  meter,  and  should  be  continued 
for  five  minutes.  An  antiseptic  dressing  is  then  inserted,  and  a  few 
days  later  the  current  is  repeated  to  destroy  any  bacteria  developed 
in  the  interim,  when  the  root  may  be  filled.  Hoffendahl  employs 
a  paste  of  paraform,  thymol,  oil  of  cloves,  and  zinc  oxide  packed  by 
means  of  asbestos  fibers. 

In  experiments  in  conjunction  with  W.  D.  Miller  they  found  0.6 
mi.  passed  for  ten  minutes  through  a  putrid  pulp  to  which  pure 
cultures  of  germs  were  added  sterilized  the  pulp  so  that  agar  cultures 
failed ;  canals  of  multi-rooted  teeth  are  best  treated  separately. 

The  principle  involved  in  immediate  sterilization  is  the  destruction 
of  all  septic  matter  within  the  canal  and  beyond  the  apex  at  the  first 
sitting. 

After  the  canal  disinfection  is  accomplished  by  one  or  more  of  the 
various  immediate  means  suggested,  its  walls  should  be  desiccated 
and  made  absorbent  by  means  of  hot  air,  then  moistened  with  euca- 
lypt(jl  or  forma-percha,  and  a  root  filling  of  temporary  stopping  or 
gutta-percha  packed  in.  If  aristol  be  added  to  these  the  eft'ect  is 
increased.  Cotton  and  forma-percha  make  a  readily  removable 
filling  suitable  to  cases  in  which  some  doubt  exists.  I  have  had  excel- 
lent results  in  molars  with  this  material  (see  p.  488.)  A  temporary 
filling  of  base-plate  gutta-percha  is  then  placed  in  the  crown  cavity  as 
a  test  filling,  or,  in  case  of  need,  the  filling  may  be  inserted. 


MOIST  GANGRENE  OF  THE  PULP  507 

Any  apical  irritation  may  he  attrihnted  to  the  tHsinfectant  and  he 
treated  hy  counterirritation,  or  the  counterirritant  may  he  aj)|)hed  as 
a  precaution  at  the  time  of  operation.  Refrigeration  of  the  <i;iim 
over  the  root  hy  means  of  ethyl  cliloride  is  a  vakiahle  means  of 
reducing  inflammation  in  these  cases.  This  traumatic  irritation  is 
often  mistaken  for  acute  septic  pericementitis.  Any  irritation  not 
too  severe  is  to  l)e  considered  as  (kie  to  non-septic  causes  and  treated 
acconhngly.  A  few  of  these  cases  may,  of  course,  result  in  failure 
owing  to  imperfection  in  the  application  of  the  methofl.  The  great 
majority  of  cases  are  successful. 

The  withdrawal  of  the  cotton  dressing  in  the  tentative  method 
should  he  done  under  aseptic  precautions.  There  may  be  found  no 
collection  upon  cotton.  In  such  case  a  fresh  twist  on  a  Swiss  broach 
should  be  passed  to  the  apex  to  determine  its  condition.  If  nothing 
l)e  found  the  root  may  be  dried  and  filled  unless  odor  be  present,  when 
the  root  should  be  resterilized  before  filling  or  the  dressing  renewed. 

Active  hemorrhage  may  ensue  or  semm  may  ooze  from  the  apical 
tissue.  This  may  be  checked  with  25  per  cent,  pyrozone,  adrenalin 
chloride,  1  to  1000,  or,  preferably,  alum  and  thymol,  and  the  root 
filled. 

If  the  apical  foramen  be  a  large  one,  and  if  a  pus  flow  follow 
the  removal  of  the  temporary  dressing  and  be  but  slight,  the  pyro- 
zone or  zinc  chloride  (or  l)oth)  should  be  used  and  the  root  filled. 
The  condition  is  one  of  apical  abscess  without  fistula,  and  is  often 
amenable  to  immediate  root  filling.  If,  however,  this  be  not  con- 
sidered advisable,  the  temporary  dressings  may  be  renewed,  though 
often  without  benefit.  Sometimes  a  thick,  glairy  fluid  will  ooze  from 
the  apical  tissue.  This  is  coagulable  lymph,  and  the  parts  require 
treatment  in  the  same  manner  as  when  a  slight  amount  of  pus  is 
present.  The  principle  involved  in  the  departure  to  an  immetliate 
method  of  treatment  is  based  upon  the  thorough  sterilization  of  the 
apical  tissue,  the  sealing  of  the  canal  to  prevent  infection  from  the 
mouth,  and  the  prevention  of  efl'usions  from  the  apical  tissue  into 
the  canal.     This  done,  the  apical  tissue  is  expected  to  care  for  itself. 

In  order  to  prevent  apical  irritation  in  so  far  as  possible,  the  gum 
is  to  be  painted  with  ordinary  tincture  of  iodine  or  spotted  with  the 
dental  tincture  of  iodine,  both  lingually  and  buccally,  as  a  counter- 
irritant. 

I^. — Iodine O'ij 

.Alcohol 5j 

Shake  frequently  for  a  week  or  two.      (Flagg.) 


508  GANGRENE  OF  THE  PULP 

If  infection  of  the  apical  tissue  by  any  chance  ensue,  either  as  the 
result  of  the  operation  of  canal  cleansing  or  previous  to  operative 
interference,  the  disease  known  as  septic  apical  pericementitis  is 
established. 

Pericementitis  following  the  opening  of  teeth  containing  gangrenous 
pulps  has  been  explained  upon  the  ground  that  the  bacteria  in  the 
absence  of  free  admission  of  oxygen  have  lost  their  virulence,  which 
is  restored  when  the  air  is  admitted.  It  is  quite  likely  that  either 
this  is  true  or  that  extraneous  bacteria  are  introduced  during  the 
course  of  treatment. 

In  case  of  partial  moist  gangrene  in  which  a  portion  of  a  filament 
is  gangrenous  and  the  balance  of  it  vital,  or  in  which  one  root  filament 
is  dead  and  the  other  vital,  the  treatment  must  be  varied  to  suit  the 
requirements.  The  dead  portion  is  removed  as  described  and  the 
living  portions  treated  as  ulcerated  pulps  (which  see,  p.  447). 

In  a  few  cases  the  continuity  of  the  canal  has  been  lost  because  it 
has  become  involved  in  caries  upon  one  side  of  the  root.  To  remedy 
this,  if  the  root  be  still  salvable,  the  cavity  should  be  excavated  and 
then  a  tapering  probe  run  through  the  tap  in  the  crown  and  into 
the  apical  portion  of  the  root  canal.  Around  this  a  non-shrinking 
amalgam  filling  may  be  built.  The  probe  is  then  withdrawn,  leaving 
a  canal  in  the  amalgam  through  which  when  hard  the  canal  may 
later  be  treated  and  filled. 

Discoloration  of  the  Teeth  by  Moist  Gangrene.— In  the  final 
decomposition  of  the  pulp  a  pigment  molecule  is  formed,  which, 
entering  the  tubules  or  formed  in  it,  stains  the  dentine  and  imparts 
an  abnormal  color  to  a  portion  or  nearly  all  of  the  crown,  which 
ranges  from  an  almost  imperceptible  loss  of  translucency  to  a 
yellow,  brown,  slaty-gray,  or  bluish  black  color.  Also  in  conditions 
of  venous  hyperemia  or  pulpitis,  with  which  venous  hyperemia 
(stasis)  is  associated,  the  escape  of  the  red  corpuscles  into  the 
tissue,  their  disintegration,  and  the  solution  of  the  hemoglobin  then 
occurs  and  the  solution  enters  the  tubules,  staining  the  dentine  a  pink 
color,  which  soon  passes  into  a  purplish  rose,  and  finally  becomes 
bluish  black  or  slaty-gray. 

Those  cases  resulting  in  the  yellowish  or  brownish  coloration  are 
usually  associated  with  the  loss  of  the  pulp  in  comparatively  sound  or 
totally  sound  teeth,  the  loss  occurring  prol)ably  through  traumatism 
or  through  slow  atrophic  changes,  such  as  occur  in  the  formation 
of  |)ulj)  nodules,  secondary  dentine,  apical  constriction,  etc.     Apical 


MOIST  GANGRENE  OF  THE  PULP  509 

abscess  is  often  much  delayed,  but  sometimes  occurs,  showing  that 
pulp  decomposition  or  a  later  infection  has  occurred.  The  demon- 
stration by  Hopewell-Smith  of  fibrosis  of  the  pulp  and  the  obliteration 
of  vascular  structures  may  account  for  a  lessened  vascularity,  and 
the  absence  of  the  production  of  iron  sulphide  because  of  the  absence 
of  necessary  putrefaction  and  the  production  of  the  hematodin 
products,  as  shown  below.  The  first  class  of  cases  occurs  either  in 
sound  teeth  in  which  the  pulps  have  died  by  traumatism,  or  in  fillerl 
teeth  with  pulps  not  exposed,  or  in  teeth  the  pulps  of  which  are  exposed 
to  the  fluids  of  the  mouth,  permitting  putrefactive  agencies  and  extra- 
neous coloring  or  color-setting  materials  to  enter.  The  discoloration 
is  most  rapid  in  the  exposed  cases. 

These  color  changes  are  rationally  explained  by  Kirk*  as  due 
to  the  decomposition  products  of  hemoglobin  existing  in  the  pulp 
at  the  time  of  its  death,  and  having  an  analogue  in  the  pigmentary 
degeneration  occurring  in  the  hemoglobin  in  a  bruise  (extravasation  of 
blood),  in  which  the  part  becomes,  first,  "black  and  blue,"  then  passes 
through  a  series  of  color  changes,  in  which  yellow,  green,  and  bluish 
black  are  notable.  These  are  due  to  new  chemical  compounds  which 
crystallize  in  the  tissue. 

These  compounds  are  divided  into  two  classes:  Hemosiderins,  or 
those  containing  iron,  and  hematoidins,  those  without  it.  Each  class 
of  these  has  several  distinct  substances  in  it,  each  having  its  own  color 
molecule. 

Kirk  states  that  methemoglobin  is  brownish  red,  hemin  bluish  black, 
hematin  dark  brown  or  bluish  black,  and  hematoidin  orange. 

Jakob  (Stengel)  gives  light  pea-green  and  brownish  red  as  the  colors 
of  hematoidin  for  an  old  hemorrhagic  focus,  showing  a  probable 
slight  chemical  variation  in  the  composition  of  the  color  molecule. 

As  the  color  changes  in  a  bruise  are  affected  imder  aseptic  condi- 
tions, and  usually  the  colors  finally  produced  are  lighter  than  the 
"black  and  blue"  first  resulting,  it  is  rational  to  suppose  that  the 
yellowish  or  brownish  discoloration  of  teeth  residts  under  such  con- 
ditions of  aseptic  decomposition  (probably  autolysis).  These  colors, 
as  remarked  by  Kirk,  are  more  or  less  permanent. 

When  a  permanent  or  progressively  darkening  slaty-gray  or  bluish 
black  color  is  produced,  it  is  considered  by  Kirk  to  be  due  to  the 
formation  of  iron  sulphide  or  an  analogous  product  in  which  iron 
and  sulphur  are  constituents,  and  that  it  is  analogous  to  the  black 

'  American  Text-book  of  Operative  Dentistry, 


510  GANGRENE  OF  THE  PULP 

discoloration  occurring  in  the  visceral  walls  of  animals  undergoing 
putrefactive  decomposition.  The  iron  is  liberated  from  the  hemoglobin 
present  by  putrefaction,  and  combines  with  the  ammonium  sulphide 
which  is  formed  from  the  ammonium  and  hydrogen  sulphide  produced 
by  the  putrefactive  decomposition. 

Treatment. — The  treatment  of  discolorations  consists  in  what  is 
known  as  the  bleaching  process,  which  means  the  reduction  of  the 
color  molecule  to  another  chemical  molecule  which  is  colorless,  and 
then  washing  that  out  of  the  tubules.  This  is  usually  done  by  the  use 
of  chemicals  which  directly  supply  a  molecule  of  nascent  oxygen  when 
coming  in  contact  with  the  putrefactive  material  or  its  product, 
the  color  molecules,  or  which,  as  chlorine,  abstracts  hydrogen  from 
the  water  present  and  so  liberates  a  molecule  of  nascent  oxygen, 
which  combines  with  the  color  molecule.  These  are  direct  or  indirect 
oxidizing  agents,  the  effect  being  the  same,  i.  e.,  an  oxidation  of  the 
color  molecule.  A  second  class,  as  sulphurous  acid,  which  abstracts 
oxygen  from  the  color  molecule,  is  called  a  reducing  agent,  and  may 
be  effective  where  the  oxidizing  agents  fail. 

In  the  use  of  bleaching  agents  the  canal  should  have  been  cleansed 
and  disinfected  with  a  simple  aqueous  solution  of  formalin  or  25  per 
cent,  ethereal  pyrozone,  or  an  aqueous  solution  of  hydrogen  dioxide, 
or  with  sodium  dioxide,  all  oils  or  other  materials  likely  to  complicate 
the  color  molecule  being  avoided.  With  the  exception  of  formalin, 
these  are  also  bleaching  agents  and  to  an  extent  aid  the  subsequent 
operation.  Formalin  would  be  best  avoided  in  cases  of  recent  pulp 
death,  as  it  may  harden  the  undecomposed  fibrils  in  the  dentine.  The 
upper  half  or  two-thirds  of  the  canal  should  then  be  filled  with  gutta- 
percha or  oxychloride  of  zinc,  leaving  the  crown  and  one-third  of  the 
root  dentine  to  be  bleached. 

After  accurate  rubber  damming  the  most  valuable  and  facile 
method  consists  of  placing  a  pellet  of  cotton  saturated  with  25  per  cent, 
ethereal  pyrozone  in  the  pulp  chamber  and  sealing  it  after  careful 
drying  of  the  lingual  tap  or  cavity  orifice  by  dropping  soft,  quick- 
setting  cement  upon  the  margin  and  sealing  the  entire  top. 

The  rubber  dam  should  not  be  removed  until  the  cement  has  set, 
as  the  ether  or  oxygen  gas  may  cause  it  to  bulge  or  blister.  This  is 
then  allowed  to  have  twenty-four  or  even  more  hours  of  action,  when, 
if  necessary,  it  may  be  removed.  The  operation  may  be  watched  at  the 
first  or  the  second  sitting  if  desired,  though  it  may  be  somewhat 
prolonged. 


MOIST  GANGRENE  OF  THE  PULP  511 

Aqueous  25  per  cent,  pyrozone  may  be  made  by  shaking  together  in  a 
test-tube  one  volume  of  distilled  water  and  two  volumes  of  25  per  cent, 
ethereal  pyrozone  and  evaporating  the  ether,  the  H2O2  being  left  in 
aqueous  solution;  the  addition  of  sodium  acetate  or  sulphate  assists 
the  passage  of  the  current.  This  is  introduced  by  means  of  the 
cataphoric  current,  the  positive  pole  being  in  the  tooth,  the  nega- 
tive at  the  hand.  Occasionally  the  reversal  of  the  poles  succeeds 
after  failure,  the  tubular  contents  probably  being  discharged  with  the 
H2O2  present  in  them. 

Oxygen  may  be  liberated  from  sodium  dioxide  (Na202)  by  sulphuric 
acid.  A  saturated  solution  of  sodium  dioxide  is  made  by  surroimding 
a  small  beaker  containing  about  2  drams  of  distilled  water  with 
cracked  ice.  AYhen  cold  the  sodium  dioxide  powder  is  to  be  slowlv 
dusted  into  it  until  it  assumes  a  semi-opaque  appearance,  indicating 
saturation.  In  use  the  dried  dentine  is  saturated  with  it,  asbestos 
fiber  being  used  to  carry  it  to  place,  and  10  per  cent,  sulphuric  acid  is 
used  to  produce  the  liberation  of  oxygen  wdth  the  following  equation : 
Na202  +  H2SO,  =  Na2SO,  +  H^O^! 

The  effervescence  forces  the  tubular  contents  out.  The  sodium 
dioxide  acts  upon  putrefactive  material,  decomposing  it,  and  also 
saponifies  fatty  matters. 

If  the  operation  fall  short  of  success,  this  is  due,  in  Kirk's  opinion, 
to  the  formation  of  iron  oxide,  which  can  be  removed  with  oxalic  acid 
by  sealing  a  crystal  of  it  in  the  pulp  chamber  for  twenty-four  hours. 

The  tubular  contents  being  entirely  removed  by  the  sodium-dioxide 
method,  the  tooth  is  more  translucent  than  by  other  bleaching  methods 
in  which  the  bleached  organic  debris  remains  in  the  tubules. 

The  chlorine  method,  introduced  l)y  Truman,  depends  for  its 
efficiency  upon  the  affinity  of  chlorine  for  hydrogen,  forming  hvdro- 
chloric  acid  (HCl).  Finding  this  in  the  water,  it  liberates  nascent  O, 
which  oxidizes  the  color  molecule,  or,  possibly,  it  abstracts  H  from  the 
organic  matter.  The  chlorine  is  usually  evolved  from  chlorinated 
lime,  that  sold  in  paraffined  paper  cartons  or  glass  bottles  being  the 
best.  That  sold  in  metal  cans  is  often  contaminated  by  the  metallic 
chlorides. 

The  dry  powder  is  packed  into  the  cavity,  moistened  with  50  per 
cent,  acetic  acid,  and  sealed  in  with  oxyphosphate  or  temporary  stopping 
for  one  or  two  days,  and  repeated  if  necessary.  Only  vulcanite,  bone, 
ivory,  or  wood  instruments  should  be  used,  as  metal  instruments  are 
acted  upon  by  the  chlorine.     All  gold  or  metallic  fillings  should  be 


512  GANGRENE  OF  THE  PULP 

removed  for  the  same  reason,  and  if  their  removal  would  cause  hard- 
ship or  so  render  the  tooth  into  a  condition  indicating  crowning, 
either  this  should  be  done  or  the  direct  oxidizing  method  tried. 

The  liberation  of  sulphurous  acid  may  be  induced  from  a  powder 
consisting  of  a  mixture  of  sodium  sulphite,  100  grains,  and  boric  acid, 
70  grains,  separately  desiccated  and  afterward  ground  together  in  a 
mortar,  by  acting  upon  it  with  a  drop  of  water.  The  cavity  is  stopped 
bv  a  plug  of  gutta-percha  previously  prepared  and  warmed.  The 
following  reaction  occurs : 

2H3BO3  +  SNa^SOj  =  2Na3B03  +  SH^O  +  SSO^ 

In  all  the  methods,  except  the  use  of  NajOj,  the  apex  of  the  canals 
should  be  sealed  before  and  after  bleaching;  at  least  1  pint  of 
hot  distilled  water  should  be  forcibly  injected  into  the  tooth  to 
dissolve  out  all  products  of  chemical  action  remaining  in  the  tubules, 
a  towel  being  used  to  catch  the  drip.  The  tooth  is  then  thoroughly 
dried,  and  if  any  organic  matter  may  be  present  in  the  tubules  the 
pulp  cavity  should  be  thinly  lined  with  oxychloride  of  zinc  to  coagulate 
it.  If  it  has  been  removed,  as  in  the  sodium  dioxide  method,  leaving 
the  tubules  empty,  they  should  be  filled  with  cavitine  varnish  after 
desiccation  to  promote  absorption,  and  the  thin  lining  then  placed. 
A  temporary  filling  is  to  be  inserted  over  this  until  success  is  evident, 
when  the  permanent  work  is  completed  with  zinc  phosphate  and  a 
metal  filling. 

The  removal  of  metallic  stains  has  been  referred  to  on  page  302. 

Moist  Gangrene  of  Pulps  of  Temporary  Teeth. — The  same  con- 
siderations pertain  to  moist  gangrene  of  the  pulps  of  temporary  teeth, 
but  as  the  roots  are  resorbed  to  some  extent  or  are  to  be  resorbed, 
the  root  filling  should  be  of  such  a  character  as  to  permit  its  resorp- 
tion. Probably  a  combination  of  paraffin  and  aristol  will  best  fulfil 
the  indications.     An  iodoform  paste  is  preferred  by  some. 

If  the  roots  be  much  resorbed,  it  is  better  to  use  a  material  which 
will  permit  venting  of  the  tooth  if  necessary.  The  canals  and  pulp 
chamber  may  be  filled  with  a  combination  of  vaseline  and  aristol,  and 
this  covered  by  a  filling.  If  trouble  arise,  a  spear  drill  is  driven  into 
the  pulp  cavity  from  a  point  beneath  the  gum  margin,  establishing  a 
vent.  The  patient  should  be  instructed  to  keep  this  open,  and  be 
furnished  a  Swiss  broach  for  the  purpose. 

At  an  age  when  the  permanent  tooth  will  shortly  thereafter  erupt, 
extraction  of  the  temporary  tooth  is  often  to  be  preferred  to  treatment. 


MOIST  GANGRENE  OF  THE  PULP  513 

Root-canal  Work  in  Cases  of  Gangrenous  Pulps  Involving 
Future  Consideration. — In  some  cases  of  douhtful  root  sterilization 

or  filling,  and  in  whicli  crowning  l)y  means  of  dowelled  erowns  is  a 
necessity,  provision  may  he  made  for  future  relief  or  treatment  by 
the  employment  of  one  of  two  excellent  methods  of  procedure: 

1.  Kirk  has  suggested  that  the  post  and  band  of  a  Richmond  crown 
be  painted  while  warm  with  a  solution  of  gutta-percha  in  chloroform. 
The  solvent  evaporates,  leaving  a  coating  of  gutta-percha.  The  crown 
is  then  set  with  cement.  By  warming  the  crown  with  a  hot  crown- 
setting  tool  (How)  or  forceps,  it  may  l)e  removed  with  ease.  The 
crown  may  be  set  with  gutta-percha  alone. 

2.  Girdwood  (Edinburgh)  has  suggested  root  intubation,  the  tul)e 
being  closed  at  the  end  with  temporary  stopping  and  then  set  with 
cement.  Immediately  thereafter  the  temporary  stopping  and  soft 
cement  are  removed  with  Donaldson  cleansers,  leaving  the  root  lumen 
free  to  the  apical  foramen  or  root  filling,  'i'he  tube  and  canal  are 
then  treated  as  a  continuous  root  canal  would  be.  The  idea  is  also 
applied  to  a  Richmond  or  all-porcelain  crown,  the  tube  being  allowed 
to  extend  through  the  backing,  to  be  later  filled  as  desired. 


33 


SECTION  V. 

DISEASES  OF  THE  PERICEMENTUM. 


CHAPTER    XIX. 
SEPTIC  APICAL  PERICEMENTITIS   (ACUTE). 

Classification. — The  dental  periosteum  and  linjamcnt,  or  the  peri- 
cementum, is  the  seat  of  numerous  nutritive  and  functional  disturb- 
ances, which  may  be  grouped,  according  to  their  causes,  into  septic 
and  non-septic. 

The  term  pericementitis  has  been  indiscriminately  applied  to  all 
affections  of  the  pericementum,  and  in  some  cases  erroneously,  for  in 
not  all  afi'ections  of  this  structure  do  the  phenomena  of  inflanunation 
appear.  However,  most  of  the  acute  and  chronic  degenerations  are 
accompanied  by  evidences  of  inflammation. 

Bodecker's  division  of  the  affections  of  the  pericementum  into  puru- 
lent and  non-purulent  is  misleading.  Cases  may  be  due  to  septic 
causes  without  pus  formation;  pus  formation  represents  but  one  form 
of  sepsis. 

The  most  convenient  clinical  classification  of  these  disorders  is  tliat 
offered  by  G.  V.  Black:*  (1)  Diseases  of  the  pericementum  beginning 
at  the  apex  of  the  root;  (2)  those  beginning  at  the  gum  margin; 
(3)  those  beginning  in  some  intermediate  portion  of  tlie  ])eri- 
cenientum.  These  may  again  be  divided,  according  to  their  causes, 
into  septic  and  non-s(<ptic.  Another  clinical  classification  wouM  be 
into  localized  and  general  disturbances — another  into  acute  and 
chronic. 

Evidences  of  Pericemental  Disturbance. — It  was  noted  in  the 
study  of  the  diseases  of  the  (h>ntal  pulp  that  the  diagnostic  signs  of 
])ulp  disturbance  were  exagg(M'ated  or  diminished  resji()ns(<  to  thermal 
stimuli;  reflected  instead  of  localized  pains;  and,  except  in  rare  cases 

'  Aniprir.in  System  of  Dentistry,  vol.  i, 


516  DISEASES  OF  THE  PERICEMENTUM 

of  advanced  degeneration,  no  tenderness  upon  percussion.  Disturb- 
ances of  the  pericementum  are  accompanied  by  entirely  different 
symptoms  which  serve  to  distinguish  between  them  and  diseases  of 
the  pulp.  They  are,  in  general,  tenderness  upon  percussion.  As 
shown  by  Black,^  the  pericementum  is  the  touch  organ  of  the  tooth, 
its  tactile  organ,  through  which  a  tooth  locates  force  applied  to  the 
tooth.  The  pains  of  pericemental  disturbance  are,  therefore,  in  the 
majority  of  cases,  exactly  localized,  instead  of  not  being  localized,  as 
in  the  case  of  the  pulp.  A  tooth  tender  upon  percussion  has  its  peri- 
cementum as  the  seat  of  disturbance.  Most  cases  of  pericemental  dis- 
eases are  accompanied  by  vascular  reactions  ranging  from  an  increased 
blood  flow  or  grades  of  hyperemia  to  pronounced  inflammation,  and 
have  the  corresponding  symptoms.  The  increased  volume  of  the  peri- 
cementum causes  the  protrusion  and  loosening  of  the  tooth,  heightened 
sensitivity  being  the  accompaniment.  As  the  vascular  supply  of  the 
pericementum  and  that  of  the  gum  are  in  a  degree  collateral  (see 
p.  175),  evidences  of  vascular  engorgement  are  seen  in  the  gum 
overlying  the  affected  tooth.  Owing  to  the  altered  density  of  the 
parts  surrounding  the  tooth  root,  percussion  upon  the  tooth  elicits 
a  different  sound  from  that  observed  in  health — the  sound  is  dull. 
The  general  symptoms  of  pericemental  affections  are,  therefore, 
tenderness  upon  percussion  and  a  dull  percussion  note,  more  or  less 
protrusion  and  looseness  of  the  tooth,  and  a  deepening  of  the  local 
gum  color. 

DISEASES  OF  THE  PERICEMENTUM  BEGINNING  AT  THE  APEX. 

Diseases  of  the  pericementum  beginning  at  the  apex  of  the  root  are 
of  two  classes,  septic  and  non-septic.  The  septic  cases  are  almost 
invariably  the  sequel  to  diseases  of  the  pulp,  namely,  suppuration  and 
gangrene,  or  arise  in  consequence  of  infection  through  the  canals  of 
pulpless  teeth.  The  non-septic  cases  are  due  to  mechanical  and 
chemical  irritants,  and  in  rare  cases  to  undiscovered  causes. 

Acute  Septic  Apical  Pericementitis;  Acute  Alveolodental 
Abscess. — Definition. — By  septic  apical  pericementitis  is  meant  an 
inflammation  of  the  apical  pericementum  due  to  the  entrance  of  septic 
organisms  into  the  tissue  lying  in  the  apical  space. 

Causes. — The  most  common  causes  of  septic  apical  pericementitis 
are: 

'  American  System  of  Dentistry,  vol.  i. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS  517 

1.  Septic  organisms  engaged  in  the  putrefaction  of  a  gangrenous 
pulp.  The  gases  and  toxic  products  evolved  by  the  process  also 
cause  much  irritation. 

2.  Pyogenic  organisms  engaged  in  the  production  of  suppuration 
of  the  pulp. 

3.  Septic  organisms  introduced  into  the  otherwise  aseptic  tissues 
of  the  apical  space  by  means  of  instrumentation  or  other  lack  of 
aseptic  precautions. 

4.  Infection  of  an  apical  space  by  an  abscess  arising  in  some  con- 
tiguous part  and  extending  in  the  direction  of  the  apical  space  under 
consideration. 

5.  Septic  infection  from  a  pyorrhea  pocket  located  upon  the  side 
of  the  tooth  in  question,  the  deepest  portion  of  which  approximates 
the  apical  space. 

6.  Possible  infection  by  way  of  the  pericemental  tract  from  the 
gum  margin  or  by  way  of  the  circulation,  which  infection  may  cause 
a  pericemental  abscess  located  in  the  apical  tissue. 

The  last  two  conditions  would  be  septic  apical  pericementitis,  but  are 
to  be  considered  separately  as  pericemental  abscess.  (See  Pyorrhea 
Alveolaris.)     As  a  cause  of  apical  abscess  it  is  rare,  but  has  been  seen. 

Apart  from  these  causes  infective  inflammation  of  apical  tissue 
does  not  seem  to  occur.  It  is  to  be  remembered  that  a  small  portion 
of  gangrenous  pulp  beneath  a  root-canal  filling  is  equivalent  to  an 
entire  gangrenous  pidp  as  a  cause  of  pericementitis.  The  vast 
majority  of  cases  occur  as  a  sequel  to  moist  gangrene  of  the  pulp, 
either  before  or  after  instrumentation  or  as  a  result  of  infection  of 
the  apical  tissue  by  instruments  either  unsterilized  or  reinfected  by 
contact  with  the  oral  fluids. 

The  organisms  found  in  acute  apical  abscesses  are  those  usually 
found  in  gangrenous  and  suppurating  pulps  and  in  a  certain  percentage 
of  even  healthy  nioutlis.  (See  p.  48.)  Schreier  found  the  Diplo- 
coccus  pneumonia^  in  fifteen  out  of  twenty  cases  examined.  He  also 
found  Staphylococcus  pyogenes  albus  and  aureus,  and  occasionally 
Streptococcus  pyogenes. 

Arkovy  found  the  Bacillus  gangrense  pulpae  in  a  number  of  cases. 
(See  p.  501 .)  These  are  virtually  the  same  organisms  that  are  found  in 
the  deeper  portions  of  a  suppurating  or  gangrenous  pulp:  this  fact  in 
itself  is  enough  to  show  the  continuity  of  infection  from  the  pulp  canal. 
It  is  a  well-known  clinical  fact  that  acute  outbreaks  of  septic  apical 
pericementitis  are  most  liable  to  occur  under  those  conditions  wlien 


518 


DISEASES  OF  THE  PERICEMENTUM 


patients  "take  cold."  Schreier  points  out  that  these  atmospheric 
states  produce  a  bodily  condition  which  favors  the  development  of 
the  Diplococcus  pneumoniae,  and  finds  in  the  association  of  these 
factors  the  reason  why  this  diplococcus  should  be  pathogenic  in  the 
dental  condition. 

Pathology,  Morbid  Anatomy,  and  Symptoms. — The  Inflammatory 
Stage. — As  in  abscess  elsewhere  there  is  first  infection  by  pyogenic 
organisms  which  produce  the  phenomena  of  infective  inflammation 
within  the  substance  of  the  apical  tissue,  and  in  the  later  stages  in 
the  contiguous  tissues. 

Fig.  420 


Showing  the  morbid  anutomy  of  sept  if  apical  pericementitis  (acute):  A,  pus;  B,  area  of 
dying  leultocytes;  C,  septic  matter  in  root  canal;  D,  excavation  of  process  (osteomyelitis); 
E,  swollen  periosteum  and  gum;  F,  alveolar  bone;  (7,  pericementum  at  edge  of  necrosis. 

Following  the  infection,  arterial  hyperemia  is  produced,  sensation 
is  exalted,  and  the  tooth  becomes  tender  upon  p(>rcussion;  but  if 
forcibly  pressed  upon — i.  e.,  if  the  arteries  be  compressed — the  hyper- 
emia is  momentarily  lessened  and  the  pressure  l)rings  a  sense  of 
relief.  At  this  stage  the  gum  over  the  apex  looks  normal,  but  may 
respond  to  pressure. 

Following  the  arterial  hyperemia,  the  venous  obstruction  which 
ends  in  stasis  is  inaugurated  and  diapcdcsisof  leukocytes  and  fibrinous 
exu(hition  into  the  intervascular  tissue  oc(;urs.  'J'lie  fixed  cells  undergo 
proliferation. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS 


519 


As  this  condition  of  inflammation  becomes  established  the  pain  dne 
to  pressure  upon  tiie  sensory  nerves  becomes  of  a  violent  throbbing 
character,  accompanied  by  a  sense  of  fulness.  The  s\vellin<r  of  the 
tissue  about  the  apex  of  the  root,  due  to  the  excess  of  fluid,  blood, 
leul^ocytes,  and  tissue  cells,  of  necessity  pushes  the  tooth  from  its  socket, 
so  that  it  feels  and  is  longer  than  the  other  teeth.  Moreover,  as  it  is 
bitten  upon  the  apical  tissue  is  further  irritated.     The  tooth  is  loosened 


Fig.  421 


Fig.  422 


Abscessed  upper  lateral.     (Skiagraph  by 
Lodge.) 

Fig.  423 


Acute  abscess  in  second  stage.  Tooth 
opened  at  b  for  treatment,  making  a  blind 
abscess.    (Black.) 

Fig.  424 


Abscess  on  crowned  root.      (Skiagraph  by 
Lodge.) 


Abscess  on  incomplete  root. 
Lodge.) 


(Skiagrarh  by 


and  percussion  induces  pain  and  elicits  the  dull  note  which  is  diag- 
nostic of  the  increase  of  bulk  in  the  pericementum.  The  color  of  the 
gum  over  the  root  becomes  deepened. 

First  Stage  of  Pus  FoRMATioN.^The  central  area  of  the  ajMcal 
tissue — i.e.,  that  next  the  apical  foramen — is  broken  (h)wn  into  pus, 
some  of  which  enters  the  root  canal  (Fig.  420,  A).  As  the  area  of 
pus  formation  widens,  all  of  the  apical  tissue  is  liquefietl  (Fig.  422,  a). 

Second  Stage  of  Pus  Formation. — The  bone  cells  become 
involved  in  the  process  and  are  destroyed  (osteitis).     The  throbbing 


520 


DISEASES  OF  THE  PERICEMENTUM 


Fig.  425 


pain,  the  extnision,  looseness,  and  dulness  to  percussion,  and  the 
inflammation  and  edema  of  the  contiguous  tissues  are  marked.  The 
gum  is  widely  inflamed,  reddened,  and  swollen,  but  no  demarcation 
of  an  abscess  may  be  noted  upon  the  gum  at  this  stage.  The  mem- 
branes of  the  adjoining  teeth  become  irritated  and  hyperemic,  and 
they  may  exhibit  tenderness  upon  percussion. 

Third  Stage  of  Pus  Formation. — The  pus  continues  to  form 
in  all  directions  until  the  bone  is  perforated  at  some  piont — i.  e., 

usually  through  the  labial  alveo- 
lar plate — that  being  the  thinnest 
and  most  readily  perforated.  The 
periosteum  is  now  destroyed  and 
the  gum  tissue  directly  involved 
as  a  boundary  to  the  pus,  which, 
collecting  beneath  it,  raises  it  into 
a  distinctly  demarked  tumefaction 
(Fig.  425,  b).  The  pain  becomes 
less  acute  owing  to  the  binding 
resistance  of  the  gum  being  less 
than  that  of  the  bone.  At  first 
the  swelling  is  hard,  and  this  rep- 
resents a  mass  of  gum  tissue  over- 
lying pus;  later,  it  softens  at  its 
highest  point,  pus  appears  as  a 
yellow  spot  beneath  the  mucous 
membrane.  The  mucous  mem- 
brane bursts  and  a  discharge  of 
pus  follows.  The  inflammation 
and  tenderness  then  largely  sub- 
side, but  some  degree  of  looseness 
and  protrusion  remains. 
During  the  latter  part  of  the  second  and  in  the  third  stage  of  pus 
formation,  instead  of  the  swelling  extending  but  little  beyond  the 
overlying  gum,  the  tissues  of  the  lips,  cheeks,  or  neck  may  be  very 
much  swollen  and  with  upper  teeth  the  eye  of  the  afl'ected  side  injected. 
In  some  cases  the  outer  skin  may  become  reddened  and  dusky,  ex- 
hibiting the  evidences  of  extension  of  the  inflammatory  process  far 
from  its  original  site. 

While  in  the  vast  majority  of  cases  the  direction  taken  by  the  pus, 
and  the  point  at  which  it  finds  exit,  is  the  buccal  or  labial  aspect,  and 


Acute  alveolar  abscess  of  a  lower  incisor  in 
the  third  stage,  with  pus  cavity  between  the 
bone  and  the  periosteum:  a,  pus  cavity  in  the 
bone;  b,  pus  between  the  periosteum  and 
bone;  c,  lip;  d,  tooth;  e,  tongue.      (Black.) 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS  521 

immediately  over  the  root  apex  of  the  affected  tooth,  or  near  it,  these 
being  the  directions  of  least  resistance,  other  anatomical  conditions 
or  histological  peculiarities  may  make  the  direction  of  least  resistance 
in  some  other  path  (Figs.  426  to  429). 

Instead  of  the  circumscribed  suppuration  described  as  the  ordinary 
course  of  abscess  formation  about  the  apices  of  roots  (septic  apical 
pericementitis)  which  accompanies  infection  by  the  staphylococci, 
clinical  evidences  of  infection  l)y  streptococci  occasionally  appear. 
The  inflammatory  process,  instead  of  being  circumscribed,  is  diffuse; 
the  inflammation  extends  along  the  lines  of  the  connective  tissues  and 
of  the  lymphatics;  the  connective  tissues  are  swollen,  the  swelling 
extending  to  the  tissues  of  the  cheek,  down  the  neck,  and  even  to 
the  shoulder — a  phlegmonous  inflammation.  Instead  of  the  com- 
paratively free  flow  of  pus  which  follows  incision  of  the  swelling  in 
ordinary  abscess,  pus  formation  in  streptococcus  infection  is  seen, 
upon  incision,  to  be  limited  and  seropurulent.  While  in  alveolar 
abscess  of  the  ordinary  types  evidences  of  septic  intoxication  or 
poisoning  are  unusual,  the  lymphatics  being  blocked,  as  a  rule,  by 
the  inflammatory  exudates,  septic  intoxication  and  poisoning  are  the 
rule  in  the  erysipelatous  cases,  those  probably  due  to  streptococcus 
infection;  bacterial  poisons  being  taken  up  by  the  lymphatics  find 
their  way  into  the  circulation. 

The  symptoms  of  the  absorption  of  bacterial  products  fi'om  the 
circumscribed  abscesses  are:  Fever,  often  ushered  in  by  a  distinct 
chill.  The  pulse  increases  in  volume  and  tension;  it  is  full,  hard, 
and  frequent.  The  tongue  is  coated,  the  bowels  constipated.  The 
patient  is  also  weakened  and  made  irritable  by  pain  and  attendant 
loss  of  sleep  and  appetite. 

In  the  streptococcal  infection  there  is  danger  that  these  may  change 
into  the  more  profound  symptoms  of  septicemia — i.  e.,  a  soft,  frequent 
pulse,  repeated  chills,  diarrhea,  clammy  skin,  general  depression,  and 
a  disordered  nervous  system. 

In  multi-rooted  teetii  the  inflammation  and  abscess  frequently  api)ear 
on  only  one  root.  If  the  case  be  .seen  early,  before  the  active  exudation 
period  of  the  inflammation  sets  in,  the  symptoms  may  be  clearly 
localized  in  one  root,  the  tooth  exhibiting  tenderness  upon  pressure 
over  the  affected  root,  but  not  upon  the  opposite  side. 

After  spontaneous  discharge  of  the  pus  from  an  abscess,  the  con- 
dition remaining  is  that  of  an  ulcerous  surface  (the  abscess  boun(hiries) 
which  is  being  continuously  infected  from  the  putrescent  pulp  rem- 


522 


DISEASES  OF  THE  PERICEMENTUM 


nants.  The  conditions,  it  is  seen,  are  not  like  those  of  ordinary  abscess, 
where  the  infective  material  is  largely  discharged  in  the  pus  evacua- 
tion, and  the  cells  bounding  the  abscess  wall  dispose  of  remaining 
bacteria,  so  that  regeneration  of  tissue  occurs.  Spontaneous  healing 
of  an  apical  abscess  is  the  exception;  the  embryonic  tissue  lining  the 
abscess  walls,  being  continuously  infected,  degenerates  and  dies  as 
fast  as  it  forms,  leaving  a  condition  known  as  chronic  apical  abscess, 
or  chronic  purulent,  apical,  septic  pericementitis. 

Clinical  History.— The  clinical  history  of  acute  alveolar  abscess  may 
be  divided  into  three  stages:  (1)  That  of  initial  inflammation  and 
pus  formation;  (2)  the  destruction  of  the  alveolar  process;  (3)  the 
passage  of  pus  through  the  periosteum  and  mucous  membrane.  The 
second  stage  is  usuallv  the  longest.     The  duration  of  the  disease 


Fig.  426 


Fig.  427 


Abscess  upon  lower  third  molar,  showing  the      Abscess  upon  palatal  root  of  an  upper  molar 
usual  paths  of  pus  exit,  A  and  B.  discharging  at  the  neck  of  the  tooth. 

depends  upon  the  readiness  with  which  the  tissues  between  the  point 
of  beginning  pus  formation  and  its  exit  yield.  When  the  pulp 
chamber  is  open  pus  may  find  exit  by  this  path,  constituting  the 
condition  known  as  blind  abscess — a  misnomer,  because  a  blind 
abscess  is  one  without  a  point  of  discharge,  without  a  fistula  leading 
to  it;  in  tlie  cases  discharging  via  the  canal,  the  latter  may  be  con- 
sidered a  fistula  (Fig.  422). 

Acute  abscesses  usually  run  a  short  course,  the  inflammatory  symp- 
toms being  .severe  and  the  tissue  destruction  limited.  Notably 
upon  lower  molars,  and  upon  the  palatal  roots  of  upper  molars, 
the  density  and  thickness  of  bone  overlying  the  roots  may  make 
paths  of  greatly  increa.sed  resistance,  so  that  the  destruction  of 
ti.ssue  proceeds  along  the  line  of  the  pericementum,  the  pus  finding 
exit  at  the  neck  of  the  tooth.     It  is  rare  in  cases  of  lower  second 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS 


523 


molars,  and  still  more  rare  ii{)on  the  tiiird  iiK^lars,  that  pus  finds 
exit  over  the  apex  of  the  root,  the  dense  bone  of  the  external  oblique 
line  offering  the  greatest  resistance  (Fig.  420).  Over  any  teeth 
the  outer  fibrous  layers  of  the  external  periosteum  may  })r(>s('nt 
unusual  resistance  to  the  pei-forative  advance  of  pus,  so  that  when 
the  fibers  of  attachment  of  the  periosteum  have  been  softened  by  the 
inflammation,  and  pus  gains  entrance  between  bone  and  periosteum, 
it  may  travel  or  l)urrow  along  the  course  of  this  membrane  (Fig.  427), 
depriving  the  bone  of  its  main  nutritive  source,  so  that  limited  necrosis 
threatens.  The  roots  of  the  central  incisors  may  lie  unusually  close 
to  the  floor  of  the  nose,  and  be  overlaid  externally  by  an  unusually 
resistant  layer  of  bone;  in  these  cases  the  path  of  least  resistance  may 


%^ 


Alveolar  abscess  at  the  root  of  a  superior  .  Alveolar  abscess  at  the  root  of  an  upper 
incisor,  discharging  into  the  nose:  a,  large  molar  discharging  into  the  antrum  of  High- 
abscess  cavity  in  the  bone;  b,  mouth  of  fis-  more:  ft,  abscess  cavity  in  the  bone;  b,  mouth 
tula  on  the  floor  of  nostril;  c,  lip;  il,  tooth,  of  fistula  on  the  floor  of  the  antrum;  c,  pus 
(Black.)  in  the  antral  cavity.      (Black.) 


be  in  the  direction  of  the  floor  of  the  nose,  the  abscess  opening  at  that 
point  (Fig.  428),  or  the  pus  may  perforate  the  lingual  alveolar  ])late, 
and,  raising  the  periosteum  and  mucous  membrane,  form  a  large 
swelling  upon  one  side  of  the  hard  palate. 

The  root  apices  of  the  posterior  upper  teeth,  particularly  of  the  first 
and  second  molars,  may,  after  the  age  of  twenty-five  or  thirty,  be 
encroached  upon  by  the  enlarging  maxillary  sinus,  so  that  any  or  all 
of  the  roots  of  these  teeth  may  be  separated  from  the  floor  of  the  sinus 
by  but  a  very  thin  lamina  of  bone  or  none;  should  abscess  arise  upon 
any  of  these  roots,  pus  discharge  into  the  antrum  woidd  necessarily 
follow.  In  these  cases  the  acute  symptoms  may  rapidly  subside,  but 
later  symptoms  of  antral  empyema  may  follow  (Fig.  429). 


524 


DISEASES  OF  THE  PERICEMENTUM 


Resort  to  the  use  of  poultices  upon  the  face,  for  the  rehef  of  the  pain 
of  abscess  formation,  may  induce  such  a  softening  of  the  tissues  over 
which  they  are  apphed  that  the  passage  of  pus  is  invited  toward  the 
exterior;  the  abscess  may  thus  open  upon  the  face  or  neck,  producing 
permanent,  disfiguring  scars  (Fig.  457). 

In  patients  who  are  in  a  cachectic  condition,  who  have  an  evil 
heredity,  or  whose  tissue  resistance  is  markedly  lessened  in  conse- 
quence of  tuberculosis,  or  more  frequently  of  syphilis,  septic  pericemen- 
titis may  run  a  riotous  course;  the  bone  suffers  extensively  by  direct 
action;  the  periosteum  is  undermined,  is  stripped  from  the  bone  over 
large  areas,  and  breaks  down  readily;  so  that  while  in  the  healthy 
person  alveolar  abscess  formation  may  run  a  direct  course  and  find 
prompt  outlet,  in  the  syphilitic  patient  extensive  pus  infiltration,  with 


Fig.  430 


Fig.  431 


Diagnosis  of  apical  abscess  by  r-rays. 
(Price.i) 


Skiagraph   of   perforation   and  apical   ab- 
scess;   wire  thrust   through  same.     (Lodge's 

metliod.) 


necrosis,  may  occur.  In  cachectic  persons  lymphatic  involvement 
is  common;  waste  products  of  bacterial  origin  find  their  way  into  the 
lymphatics,  and  set  up  secondary  irritative  processes  in  the  nearest 
lymphatic  glands — lymphadenitis. 

In  persons  whose  oral  hygiene  is  neglected  the  third  stage  of  alveolar 
al)scess  is  frefjuently  violent  and  the  inflammatory  process  widespread. 

Diagnosis. — In  incipient  apical  ])ericementitis  the  symptoms  may 
consist  of  reflex  pains,  but,  as  a  rule,  are  distinctly  localized  in  the 
teeth  aft'ected,  which  are  tender  to  the  touch.  The  discoloration  of 
the  tooth  crown  and  other  evidences  of  moist  gangrene  are  usually 
present  unless  the  tooth  has  been  previously  partially  treated,  when 
the  color  may  be  good,  but  by  transmitted  light  opacity  is  noted. 
In  the  j)n)iif)unc('(l  cases  the  symptoms  are  as  described. 


Itf'iiisof  IiiteroHt,  1901. 


ACUTE  SEPTIC  APICAL  PERICEMEXTITIS  525 

After  high  inflammation  has  existed  for  twenty-four  hours,  pus  is 
generally  present  in  the  apical  tissue. 

Of  two  pulpless  teeth  surrounded  by  a  zon(>  of  inflammation,  the 
most  tender  is  the  one  affected,  though  l)otli  may  be  acting  at  once. 
It  is  to  be  remembered  that  adjoining,  otherwise  normal,  teeth  may 
show  some  evidence  of  pericementitis,  so  that  differentiation  is  neces- 
sary. The  various  stages  of  inflammation  and  pus  formation  are 
judged  by  the  appearance  of  the  gum  or  by  the  a:-rays  (Fig.  480).  The 
greater  the  swelling  and  injection  of  the  gum,  the  more  advanced  is 
the  pus  formation. 

The  inflammatory  action  precedes  the  advance  of  pus,  which 
furnishes  a  guide  to  the  direction  the  pus  is  pursuing — viz.,  where 
the  most  intense  coloration  and  the  greatest  swelling  appears  will  be 
the  point  at  which  the  abscess  will  point  or  di.scharge.  A  sudden 
subsidence  of  inflannnation  without  an  innnediately  discoverable 
point  of  pus  exit  should  lead  to  the  suspicion  that  the  discharge  has 
taken  place  in  an  imiisual  situation. 

An  abscess  originating  about  an  impacted  tooth,  or  one  due  to 
subperiosteal  inflammation,  must  be  differentiated.^ 

A  pericemental  abscess  must  also  be  considered.  An  acute  abscess 
of  the  pulp  in  its  most  pronounced  stage  may  simulate  incipient  or  even 
pronounced  acute  apical  pericementitis.     (See  p.  450.) 

The  last  three  conditions  are  usually  associated  with  suspected 
teeth  containing  vital  pulps,  so  that  tests  for  pulp  vitality  are  to  be 
applied. 

In  certain  cases  of  pulp  gangrene  part  of  the  pulp  only  may  be 
dead — e.  g.,  the  lingual  filament  of  the  pulp  of  an  upper  molar;  while 
the  balance  may  be  vital  (the  buccal  filaments).  This  fact  may  con- 
fuse the  response  to  tests  and  is  to  be  borne  in  mind. 

Prognosis. — In  the  majority  of  cases  the  prognosis  of  acute  apical 
abscess,  as  to  the  future  retention  of  the  tooth,  is  favorable;  and  usually 
very  favorable  if  the  case  receive  intelligent  therapeutic  aid.  The 
future  of  the  tooth  depends  upon  the  thoroughness  with  which  sources 
of  infection  may  be  destroyed  and  permanently  removed  and  the 
completeness  with  which  regeneration  of  tissue  can  be  induced. 

Treatment. — In  the  initial  inflammation  and  first  stage  of  pus  for- 
mation the  treatment  should  be  abortive.  The  cause  of  the  inflamma- 
tion should  be  removed,  if  possible,  and  the  pus  formed  be  removed  or, 
at  least,  permitted  to  escape  by  way  of  the  pulp  canals.     The  prompt- 

'  Black,  .\merican  System  of  Dentistry,  vol.  i. 


526  DISEASES  OF  THE  PERICEMENTUM 

ness  of  relief  from  pain  depends  upon  the  thoroughness  with  which 
this  is  accomplished. 

The  pulp  chamber  should  be  opened  to  an  extent  which  permits 
the  free  passage  of  broaches  into  the  canal  (Figs.  422  and  427). 

If  the  cavity  of  decay  be  open,  the  pulpal  wall  is  to  be  perforated. 
If  a  filling  be  present,  it  is  in  part  or  entirely  remoyed.  If  the  enamel 
be  entirely  sound,  or  if  subsequent  treatment  require  a  new  opening 
in  line  with  the  pulp  canals,  it  is  at  least  in  part  made. 

These  openings  are  usually  begun  with  a  small,  spear-pointed  drill 
(So.  100  S.  S.  W.  Catalog)  revolving  in  a  perfectly  true  hand  piece. 
To  centre  the  drill,  first  spot  the  enamel  with  a  dentate  bur.  The 
opening  made  is  enlarged  with  successive  sizes  of  sharp,  round, 
dentate  burs  until  of  sufficient  size. 

According  to  the  amount  of  tenderness,  the  tooth  will  require  a 
counterpressure  to  that  of  the  drill.  If  the  entrance  be  made  through 
the  occlusal  face  of  the  tooth,  or  in  a  direction  which  would  cause 
direct  pressure  on  the  apical  pericementum,  a  ligature  of  linen 
thread  with  long  ends  may  be  placed  around  the  tooth,  and  traction 
be  made  by  drawing  on  the  loose  ends  of  the  ligature.*  Effective 
counterpressure  against  lateral  entrance  to  the  pulp  chamber  may 
be  made  by  softening  a  small  roll  of  modelling  compound  and  mould- 
ing over  the  face  of  the  affected  tooth  and  several  of  those  adjoining 
it,  and  hardening  with  cold  water.  This  temporary  splint  is  held  in 
place  by  the  index  finger  of  the  left  hand.  In  case  the  inflammatory 
process  is  marked,  or  if  the  patient  be  in  bed,  it  may  be  necessary 
to  make  a  vent  opening  by  the  easiest  path,  especially  when  using  a 
hand  drill — i.  e.,  at  the  junction  of  enamel  and  cementum — directly 
into  the  chamber. 

As  soon  as  entrance  to  the  pulp  chamber  is  effected,  the  cavity  is 
syringed  with  a  strong  antiseptic.  Fine  probes  are  passed  and  repassed 
into  the  opening  to  free  the  outlet,  so  that  gases  may  escape  and  fresh 
portions  of  the  antiseptic  be  worked  into  the  cavity.  The  quickness 
with  which  relief  is  secured  will  depend  upon  the  thoroughness  with 
which  the  canals  are  entered  and  their  putrid  contents  given  vent.  A 
tedious  class  of  cases  are  those  in  which  a  canal  of  a  molar  is  filled 
or  [)artiHlly  filled.  ITidess  entrance  to  and  cleansing  of  the  canal 
be  accomplished,  the  inflamniution  will  proceed  until  the  pus  finds 
external  vent.  An  hour  sjK-nt  in  gaining  access  to  and  cleansing  such 
canals  is  well  spent. 

'  J.  Foster  I'lagg,  Lenturew  on  Dontal  TViorapputics. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS  527 

The  canals  may  be  dried  and  an  anodyne  antiseptic,  such  as 
phenol  camphor  plus  menthol,  pumped  into  them.  If,  now,  pro- 
vision against  mastication  upon  the  elongated  tooth  be  made  by 
means  of  a  guard,  relief  is  tolerably  certain. 

Watkins^has  used  "blue  light"  as  applied  from  a  16  candle  power 
bliie-glol)ed  electric  lamp  through  a  funnel  directly  upon  the  part.  He 
claims  relief  from  the  pain,  enabling  him  to  open  the  tooth  previously 
too  painful  to  be  operated  upon.  He  also  claims  that  swelling  is 
much  reduced  by  it,  in  some  cases  in  twenty  minutes. 

If  desired,  small  apical  abscesses  may  be  treated  by  the  Zierler- 
Hoffendahl  method  used  for  gangrene  pulps.    (See  p.  505.) 

Probably  it  is  better  to  vent  as  indicated  and  to  treat  later,  except 
in  such  cases  as  do  not  present  any  acute  symptoms.  Patients  do 
not  ordinarily  tolerate  the  rubber  dam  in  these  cases. 

A  guard  may  be  made  from  a  strip  of  rubber  dam  two  inches  long 
and  of  a  width  corresponding  to  the  distance  from  the  buccal  to  the  lin- 
gual gum  margins  and  folded  into  a  pad  of  the  width  of  the  occlusal 
face  of  the  tooth  to  be  covered.  Floss  silk  is  then  sewed  through  this 
in  such  a  manner  as  to  cause  it  to  tie  the  pad  over  the  tooth,  the  silk 
itself  encircling  the  neck  of  the  tooth.'  This  should  be  attached  to  a 
nearby  tooth,  and  will  insure  rest  of  the  affected  pericementum  by 
preventing  occlusion  upon  the  crown  (Fig.  432). 

A  mixture  of  tincture  of  aconite  and  tincture  of  iodine,  or  dental 
tincture  of  aconite,  should  be  then  painted  upon  the  gum  over  the 
tooth. ^  The  inflammation  usually  subsides  and  almost  disappears  in 
a  couple  of  days.  The  local  measures  should  be  supplemented  in 
somewhat  severe  cases  by  the  administration  of  a  saline  cathartic  or 
the  hot  pediluvium  as  derivatives.  Instead  of  catharsis,  the  hot  ])edi- 
luvium  and  (Ha})horesis  may  be  conjoined;  10  grains  of  Dover's 
powders  in  hot  lemonade  are  to  be  taken  after  the  pediluvium'  and 
the  patient  well  covered  up  in  bed.  These  several  measures  are  to  be 
regarded  as  the  abortive  treatment  of  alveolar  abscess;  they  apply  to 
all  cases  if  seen  early  enough,  and  will  in  the  majority  of  cases  prevent 
the  disease  of  the  pericementum  passing  the  early  inflannnatory  stages. 

1  Dental  Cosmos,  1905.  =  Flagg. 

•■'  Dental  tincture  of  aconite  may  be  made  by  cvapnratinR  the  official  tincture  to  one- 
fourth  its  bulk.  It  should  be  used  with  great  care,  and  be  covered  for  one-half  hour  with 
a  i>ad  of  cotfonoid.  The  patient  should  be  cautioned  against  swallowing  the  saliva  during 
this   time.      (FlaKs.) 

■*  Endclman  (Dental  Cosmos,  March,  1904)  suggests  the  rational  improvement  of  immersing 
the  feet  in  warm  water  which  is  gradually  made  hotter,  as  bearable,  until  the  ves-sels  of  the 
feet  become  well  engorged. 


528 


DISEASES  OF  THE  PERICEMENTUM 


In  all  cases  the  severity  of  the  inflammatory  process  is  lessened  in 
proportion  to  the  thoroughness  with  which  the  antiseptic  measures 
are  applied,  provided  that  in  the  attempt  at  such  application  no  septic 
matter  be  violently  thrust  through  the  apical  foramen. 

While  this  is  true,  marked  relief  is  so  often  given  in  even  severe  cases 
by  the  simple  opening  of  the  pulp  chamber  by  means  of  a  spear  drill, 
thus  permitting  the  gases  and  pus  to  find  vent,  that  in  those  cases  in 
which  tenderness  of  the  tooth  prevents  thorough  opening,  or  when 
patients  are  confined  to  bed  by  illness,  such  an  opening  may  be  made, 
either  at  the  neck  of  the  tooth  or  through  a  filling. 

In  the  second  stage  of  pus  formation  the  abortive  treatment  may 
still  be  attempted.  In  some  cases  this  is  successful  in  at  least  reducing 
the  acute  pain  which  demoralizes  the  patient. 


Fig.  432 


Fig.   434 


o  O 


Rubber  dam  guard  for  use  in  pericemen- 
titis: A,  roll  of  dam  threaded;  B,  guard  fitted 
over  tooth;  tooth  eliminated  to  show  the 
manner  in  which  the  silk  encircles  it. 


Walker-Younger 

trephines. 


If  the  pain  persist,  the  gum  and  bone  overlying  the  apical  space 
should  be  perforated  in  order  to  form  an  artificial  fistula. 

Black's  method  is  a  good  one.  A  few  drops  of  carbolic  acid  are 
placed  on  a  glass  slalj  and  a  deeply  serrated  plugger  point  is  dipped 
into  this,  and  the  tiny  drop  adherent  is  laid  upon  the  gum,  which  it 
eschars  and,  in  part,  anesthetizes.  The  serrated  point  is  used  to 
scratch  the  escharred  tissue;  more  carbolic  acid  is  added  and  the  pro- 
cess repeated  until  the  bone  is  reached.  A  fresh  drop  is  then  placed 
and  the  bone  perforated  with  a  sharp  chisel  or  a  spear  drill.  The 
location  of  the  al)scess  may  sometimes  be  determined  by  measuring 
the  length  of  the  root  by  the  use  of  a  Donaldson  hook,  over  the 
shank  of  which  a  disk  of  rubber  dam  has  been  passed  as  a  guide. 

The  gum  may  be  refrigerated  with  ethyl  chloride,  or  a  little  cocaine 


ACUTE  SEPTIC    APICAL   P  ERIC  EM  EXT  IT  IS  529 

solution  may  be  injecU'd  into  it,  and  a  deep  cut  l)c  made  to  the  hone, 
after  which  the  perforation  of  the  bone  is  made.  After  cocainizing 
the  parts  a  Rollins  tubular  knife  may  be  used  to  remove  a  circular 
section  of  gum  tissue,  after  which  a  fine  trephine  or  tiie  drill  may  be 
employed  to  enter  the  apical  space.  The  difficulty  of  determining  the 
exact  location  of  the  abscess  seat  renders  this  operation  of  perforation 
almost  impracticable  in  some  cases.  Under  such  circumstances  the 
abortive  treatment,  both  local  and  systemic,  must  be  made  as  thor- 
ough as  possible,  and  if  not  successful  the  patient  may  be  kept  under 
the  influence  of  morphine  until  such  time  as  the  pus  formation  has 
reached  the  third  stage.  This  may  be  hastened  by  the  use  of  a 
capsicum  plaster  applied  to  the  gum.  This  may  properly  be  denomi- 
nated the  expectant  treatment,  and,  while  perhaps  unsurgical,  presents 
at  times  no  alternative  but  tooth  extraction. 

As  a  preventive  of  possible  blood  infection  the  following  may  be 
administered: 

I^. — Hydrargyri  bichloridi gr.  j 

Tinct.  ferri  chloridi f5j — M. 

Sig. — Twenty  drops  in  water  four  times  a  day. 

The  editor,  while  suffering  from  a  very  severe  abscess  about  the 
finger  nail,  due  to  infection  by  the  Strej)tococcus  pyogenes  anil  asso- 
ciated with  lymphangitis  extending  as  a  bright  red  streak  into  the 
axilla,  employed  this  remedy  with  markedly  beneficial  effect. 

In  case  the  patient  suffer  marked  physical  debility,  owing  to  pain 
and  intestinal  disturbance,  a  stimulant  tonic  should  be  used  after  the 
use  of  the  saline  cathartic. 

I^.— SaloH, 

Quinine  suipliatis afi     gr.  xxx. 

M.  et  fiant  capsuke  No.  x. 

Sig. — Take  one  capsule  before  each  meal  and  on  retiring. 

Tablets  containing  salol  antl  quinine,  2^  grains  each,  may  be  had 
of  dniggists. 

This  combination  acts  as  tonic,  antipyretic,  and  antise])tic. 
The  following*  is  also  suggested  as  analogous: 

I^. — (.iuininx  sulphatis gr.  .\.\x 

Acetanilide gr.  xxiv 

Caffeina;  citratis gr.  iij. 

M.  et  fiant  pil.  No.  xij. 

Sig. — One  everj'  liour. 

In  the  third  stage  the  pus  is  in  the  tissues  exterior  to  the  alveolar 
process.     A  deep,  free  incision  should  be  made  in  order  to  evacuate 

1  llndolnian,  Dental  Cosnio.s,  1904. 

34 


530  DISEASES  OF  THE  PERICEMENTUM 

the  abscess;  a  methyl  chloride  spray  or  a  cocaine  injection  being  used 
as  an  anesthetic  in  those  cases  in  which  the  pus  is  deep  seated. 

The  abscess  cavity  is  then  to  be  syringed  out  with  hamamelis 
(distillate)  and  afterward  with  hydrogen  dioxide. 

It  has  been  recommended  that  at  this  time  the  root  end  be  sc  aped 
or  amputated  as  a  means  of  insuring  the  cure  of  the  abscess.  There 
can  be  no  objection  to  the  removal  of  shreds  of  necrotic  tissue  about 
the  root  apex,  nor  even  to  slight  amputation  if  the  operation  be 
endurable.  The  great  majority  of  these  cases  are,  however,  curable 
by  correct  root-canal  treatment,  and  the  inflammatory  symptoms  and 
conditions  under  which  one  operates  seem  to  indicate  that  a  better 
course  is  to  introduce  a  drain  of  antiseptic  gauze  into  the  abscess 
cavity  through  the  incision  in  order  that  the  fistula  shall  not  close 
externally.  The  tent  of  gauze  should  not  be  left  more  than  twenty- 
four  hours,  or  the  surrounding  clot  may  so  enclose  it  that  the  pus  will 
not  drain  properly,  a  second  enclosure  of  pus  thus  ensuing.  The 
patient  should  be  instructed  to  remove  it  if  such  symptoms  appear. 
This  is  necessary  only  when  the  pus  has  been  deep  seated  and  a  fair 
amount  of  tissue  has  been  penetrated  to  reach  the  abscess.  Upon 
the  cheek  should  be  placed  compresses  wet  with  an  antiphlogistic. 

I^. — Liquor  plumbi  subacetatis f  3iv 

Tinct.  opii Bj 

Aquae Oj — M. 

Cataplasma  kaolini  (official)  (composed  of  kaolin,  boric  acid, 
glycerin,  methyl  salicylate,  thymol,  and  oil  of  peppermint)  may  be 
spread  upon  linen  and  applied  to  the  part. 

The  root  canals  need  not  necessarily  be  opened  at  this  time.  In  a 
day  the  intense  inflammatory  symptoms  should  have  subsided. 
If,  later,  the  treatment  for  chronic  abscess  be  not  successful,  the 
abscess  cavity  may  be  packed  open  with  antiseptic  gauze  and  the  root 
end  amputated  under  conditions  vastly  more  favorable  to  success. 
(See  Treatment  of  Chronic  Apical  Abscess.) 

As  a  means  of  reducing  swelling,  vibratory  massage  is  useful.  A 
simple  appliance  for  this  purpose,  devised  by  W.  H.  Mitchell,*  con- 
sists of  a  cam-like  piece  of  metal  perforated  at  its  smaller  end  for 
mounting  upon  a  screw  mandril;  it  is  held  in  the  dental  hand  piece 
strapped  to  the  hand  as  shown.  Its  centrifugal  force  imparts  a 
vibratory  motion  to  the  hand  which  can  be  utilized  for  massage  with 
the  finger  tips,  or  by  holding  in  the  hand  an  instrument  containing 

'  Dciit;.  1   Brief,   1908;    Academy  of  Stoiuatolcjgy. 


ACUTE  SEPTIC  APICAL  I'EIilCEMENTITIS 


531 


upon  its  end  a  soft  rubber  cup.     The  part  to  be  massaged  should 
be  lubricated  with  vaseline. 

Fig.  435 


W.  H.  Mitc)ieirs  vibrator  and  rubber  caii  applicator. 

Under  no  circumstances  should  hot  poultices  be  applied  to  the  out- 
side of  the  face,  as  a  discharge  of  pus  in  that  direction  will  cause  a  dis- 
figuring scar.  If  an  abscess  threaten  to  open  externally,  the  abscess 
should  be  opened  by  an  incision  made  from  a  point  within  the  mouth, 

Fio.   430 


W.  H.  Mitchell's  vibrator  strapped  to  the  hand. 

and,  after  sterilization  of  the  tract,  a  drainage  tent  of  antiseptic  gauze 
should  be  introduced  nearly  to  the  bottom  of  the  pus  cavity.  This 
should  be  removed  daily,  the  abscess  cavity  sterilized,  and  the  tent 


532  DISEASES  OF  THE  PERICEMENTUM 

renewed.  An  antiphlogistic  compress  should  be  applied  to  the  face. 
The  principal  object  sought  is  the  mechanical  apposition  of  the  walls 
of  the  abscess  cavity  at  the  dependent  or  external  portion,  in  order 
that  these  shall  unite  by  granulation  and  that  the  fistula  shall  in  this 
manner  become  an  ordinary  one.  The  patient  should  lie  in  a  position 
to  counteract  the  natural  effect  of  gravitation. 

After  lancing,  the  mouth  should  be  kept  well  sterilized  by  frequent 
sprays  or  gargles  of  hydrogen  dioxide,  which  may  be  diluted  to  one- 
third  strength  with  water — i.  e.,  to  a  1  per  cent,  solution. 

If,  in  connection  with  the  lower  third  molar,  marked  swelling  be 
observed  in  the  submaxillary  triangle,  free  incision  of  the  tissues  of 
the  floor  of  the  mouth  should  be  made  at  the  angle  of  junction  with 
the  bone.  The  cut  should  be  made  close  to  the  bone  and  toward  it, 
but  not  too  deep,  lest  the  mylohyoid  artery  or  nerve  be  injured. 

The  deep  lancing  of  an  abscess  upon  the  hard  palate  may  cause 
a  cut  to  be  made  in  the  posterior  palatine  artery.  External  to  the 
lower  jaw  the  facial  artery  is  to  be  considered.  Keeping  close  to  the 
alveolar  process  while  the  cheek  is  pulled  out  renders  the  operation 
safe. 

It  is  ever  to  be  borne  in  mind  that  so  long  as  the  source  of  infection 
remains  pus  formation  continues,  and  so  long  as  pus  forms  tissue 
destruction  is  in  progress;  furthermore,  in  proportion  to  the  amount 
of  tissue  loss  perfect  recovery  after  alveolar  abscess  is  delayed  or 
imperfect. 

While  it  is  the  clinical  experience  of  nearly  every  operator  that  a 
tooth  and  adjacent  structures  may  recover  from  inflammation  which 
involves  not  only  the  first  tooth  attacked,  but  by  an  extension  of  the 
inflammatory  process  involves  the  general  periosteum  and  neighboring 
teeth,  provided  the  case  receive  prompt  and  decisive  surgical  treatment, 
yet  the  danger  of  necrosis  and  septicemia  in  prolonged  cases  is  always 
imminent.  When  the  general  periosteum  is  involved,  as  shown  by 
extensive  boggy  swelling  in  the  mouth,  if  several  free  incisions  carried 
to  the  bone  do  not  afford  j)rompt  relief,  the  tooth  which  is  the  centre 
of  infection  should  be  promptly  extracted.  If,  in  the  contiiuied  course 
of  the  pericementitis,  chills,  followed  by  fever,  a  coated  tongue,  and 
nmch  physical  depression  occur,  a  general  infection  is  to  be  feared, 
and  no  time  should  be  lost  in  sterilizing  the  mouth,  extracting  the 
tooth,  and  subjecting  the  socket  to  free  spraying  with  antise})tics. 

I(  liiis  been  a  subject  of  controversy  whether  a  tooth  should  be 
extracted  while  the  abscess  is  forming.     It  has  been  claimed  that  the 


ACUTE  SEPTIC  APICAL  PERICEM EXTITIS  :^:Y.\ 

contimiiition  of  pus  formation  after  extraction  rendei-.s  tlie  state  of  the 
patient  even  worse  than  before  extraction. 

This  occurrence  is  comparatively  infrequently  seen,  and  is,  of  course, 
due  either  to  the  retention  of  some  pyogenic  organisms  beneath  the 
clot  which  forms  in  the  alveolus  or  the  infection  of  the  parts  by  ex- 
traneous organisms. 

The  retention  of  the  tooth  until  a  fistula  forms  would  also  confine 
the  bacteria  for  the  time. 

Unquestionably  metastatic  infections  have  appeared  as  the  result 
of  persistent  local  infection  following  tooth  extraction,  the  avenue 
being  the  lymphatics;  therefore,  in  cases  of  extraction  during  the  second 
stage  of  pus  formation,  the  alveolus  should  be  forcibly  syringed  for 
ten  minutes  with  hydrogen  dioxide,  in  every  four  ounces  of  which 
1  grain  of  mercuric  chloride  has  been  dissolved.  If  it  be  thought 
desirable  to  repeat  the  syringing,  a  tent  of  antiseptic  gauze  may  be 
gently  carried  to  the  apex  of  the  alveolus  and  left.  This  tent  may  be 
removed  to  permit  syringing,  and  should  never  be  left  long  at  any  one 
time,  as  septic  inflammation  of  the  alveolar  walls  may  occur.  It  also 
does  not  drain  pus  readily,  so  it  might  cause  an  abscess  if  left  too  long. 

In  cases  of  this  kind  oral  sterilization  and  anti-infective  systemic 
medication  are  of  importance.  As  soon  as  improvement  is  noted  the 
tent  should  be  removed,  the  alveolus  sterilized  as  before,  and  a  new 
clot  induced  by  a  curetting  of  the  walls.  The  case  should  now  ])i-o- 
ceed  as  any  ordinary  extraction. 

In  a  reply  to  a  circular  letter  of  questions  regarding  this  point, 
Black,  Kirk,  Ottolengui,  Hofi'heinz,  and  Schamburg  all  favored 
extraction  as  a  means  of  removal  of  the  cause  and  as  a  less  evil  than 
allowing  the  tooth  to  remain  enclosing  the  bacteria,  which,  if  capable 
of  producing  septicemia,. it  would  do  if  allowed  to  remain.  They  are 
therefore  in  agreement  with  the  editor's  position  taken  in  the  second 
edition  of  this  work  (1904).  Brown  argues  the  difficulty  of  decision 
in  an  individual  case.  All  are  practically  opposed  to  the  idea  that 
pneumonia  is  more  likely  to  result  from  post-extraction  sepsis  rather 
than  septicemia,  Morris^  having  tak(>n  the  position  that  jJUiMiinoin'a 
resulted  from  extractions  in  this  condition.  P^ach  and  all  advised 
careful  ante- and  post-t»xtraction  antisepsis. 

The  editor  has  had  quite  a  number  of  cases  of  necrosis  following 
extractions  at  the  hands  of  specialists,  and  believes  they  and  he  should 
have  been  more  watchful  in  these  cases,  and  that  in  most  cases  the 

'  Mitchell.  Dental  Cosmos,  1907,  p.  713. 


534  DISEASES  OF  THE  PERICEMENTUM 

antiseptic  spraying  of  the  alveolus,  etc.,  is  a  reliable  measure.  The 
making  of  a  cautious  diagnosis  and  awaiting  the  proper  time,  as 
recommended  by  IMitchell,  is  a  physical  impossibility  unless  one 
await  the  third  stage  or  a  fistula  or  general  infection,  as  in  this  state 
the  bacteria  are  considered  virulent,  especially  while  bone  solution 
is  in  progress. 

In  cachectic  individuals  acute  abscesses  may  cause  inflammation  of 
the  deeper  tissues  and  of  the  periosteum  as  well,  and  extensive  necrosis 
may  occur. 

Acute  septic  apical  pericementitis  may  occur  on  a  temporary  tooth, 
most  frequently  a  temporary  molar.  The  symptoms  and  pathology 
are  the  same,  except  that  the  looser  character  of  the  alveolar  structure 
seems  to  frequently  permit  the  abscess  to  assume  the  chronic  form 
before  the  dentist  is  consulted.  Children  often  hide  these  conditions 
from  their  elders  out  of  fear  of  the  dentist.  In  strumous  children  the 
inflammation  may  be  spreading  and  the  lymphatic  glands  may  be 
involved.  There  may  also  be  some  symptoms  of  septic  intoxication 
evidenced  by  chills  accompanied  by  fever,  etc.  These  cases  require 
an  opening  of  the  abscess,  sterilization  of  the  part,  and  attention  to 
the  systemic  condition.  If  seen  in  the  acute  stage  the  treatment  is 
the  same  as  for  the  permanent  teeth,  unless  the  disease  occur  shortly 
before  the  date  for  eruption  of  the  permanent  successor,  when  the 
temporary  tooth  should  be  extracted.  If  treated,  the  canals  should 
be  filled  with  materials  which  can  be  resorbed  by  the  tissues,  such 
as  paraffin  or  wax  with  aristol. 

As  soon  as  the  pus  escapes,  the  condition  of  chronic  apical  abscess 
is  established. 


CHAPTER    XX. 

CHRONIC  SEPTIC,  PURULENT,  APICAL  PERICEMENTITIS 
(CHRONIC  APIC.\I.  ABSCESS). 

By  this  title  is  meant  a  condition  of  apical  pericementitis  due  to 
septic  influences  in  which  pus  is  continuously  formed  at  the  expense 
of  the  apical  pericementum  and  contio;uous  tissues.  It  is  the  usual 
outcome  of  acute  apical  abscess,  and  is  established  as  soon  as  the 
pus  finds  vent  either  through  the  gum  as  a  natural  or  operative  result, 
or  through  the  root  canal  as  the  result  of  opening  the  canal. 

These  two  avenues  of  pus  escape  give  the  two  clinical  conditions  of 
(1)  chronic  apical  abscess  discharging  via  the  root  canal;  (2)  chronic 
apical  abscess  with  fistula. 

CHRONIC  APICAL  ABSCESS  DISCHARGING  VIA  THE 
ROOT  CANAL. 

Pathology  and  Morbid  Anatomy. — First  Grade. — Upon  abortion  of 
an  acute  abscess  in  the  first  stage  the  pressure  of  pus  upon  the  a])ical 
tissues  is  released,  and,  as  a  rule,  the  walls  of  the  abscess  cavity  throw 
out  granulations  which  fill  it.  This  tissue  tends  to  organize  into  more 
or  less  healthy  tissue  (cicatricial  tissue).  The  bacteria  are  killed  out 
except  at  that  part  represented  by  immediate  contact  with  the  root 
foramen;  at  this  point  the  tissues  are  infected  and  some  molecular  loss 
of  tissue  as  pus  may  occur.  A  limited  loss  of  granulation  tissue  lu- 
pus formation  is  compensated  for  by  the  formation  of  new  granu- 
lations. The  conditions  are  almost  analogous  to  those  existing  in 
moist  gangrene  of  the  pulp,  and  require  analogous  treatment. 

Second  Grade. — If  the  abortion  of  the  abscess  have  only  j)artly 
permitted  the  pus  to  drain,  or  the  alveolar  walls  or  crypts  of  the  abscess 
wall  remain  infected,  the  pus  will  continue  to  form  and  escape  in 
some  degree  via  the  canal.  If  the  tooth  now  be  extracted,  a  small 
abscess  sac  will  be  found  upon  the  root  end.  If  opened,  this  will  be 
.seen  to  be  a  mass  of  fibrous  vascidar  tissue  (inflamed  ])ericemental 
apical  tissue)  having  a  central  lumen  connecting  with  the  root  canal 
(the  abscess  cavity). 


536  DISEASES  OF  TflE  PERICEMENTUM 

Third  Gr.'U)e. — AYith  partial  vent  to  the  pus  formed,  the  abscess 
cavity  of  the  second  grade  may  enlarge,  involve  the  bony  walls  of 
the  alveolus,  and  the  soft  tissues  then  proliferate  to  such  an  extent  that 
they  finally  organize  into  a  large,  fibrous,  vascular  sac  attached  to  the 
tooth.  This  sac  has  the  central  pus  cavity  before  described,  which 
is  connected  with  the  pulp  canal.  It  may  be  a  half-inch  or  more  in 
length  (Fig.  437)  and  may  be  extracted  with  the  tooth  or  may  be  left 

attached  to  the  bone.     It  necessa- 
^^^-  4^''  rily  occupies  in  the  latter  a  cavity 

of  a  size  corresponding  to  its  own 
bulk.  As  its  inner  walls  are  in- 
fected, extraction  without  its  re- 
moval leaves  an  infected  area, 
which  must  be  disinfected  or  a  sec- 
ondary acute  abscess  may  result. 
Fourth   Grade. — Instead   of 

Chronic  apical  abscess,  third  grade:  5,  ab-  organizing,  theflbrOVaSCular  tisSUC 
scess  sac  containing  a  central    pus  cavity;  D,  it  c     ^    •  rm 

apex  of  root;  C,  canal  containing  pus.  may    be    liquchcd    Hlto  pUS.        i  hc 

root  apex  becomes  denuded  for  a 
distance  about  the  apical  foramen.  Pus  collects  about  the  apex  of 
the  root  and  rests  upon  the  bone,  owing  to  the  influence  of  gravity. 
The  bone  is  thus  infected,  inflamed,  and  further  liquefied,  while 
necessarily  the  abscess  cavity  enlarges.  If  a  bistoury  be  thrust  through 
the  labial  alveolar  wall  in  such  a  case,  as  shown  in  Fig.  438,  but  slight 
resistance  will  need  to  be  overcome.  In  the  lower  jaw  the  tendency 
is  to  burrow  into  the  cancellated  tissue  of  the  bone  away  from  the  tooth, 
so  that  destruction  of  the  pericementum  may  not  be  very  extensive. 
In  the  upper  jaw  tlie  tendency  is  to  spread  along  the  pericementum 
and  into  the  cancellated  bone,  so  that  the  cavities  of  chronic  abscess 
upon  the  upper  anterior  teeth  particularly  may  cause  extensive  excava- 
tion in  the  palatal  process  of  the  superior  maxillary  bone  (Fig.  440). 
The  pus  may  burrow  in  irregular  a)id  circuitous  directions,  until  it 
finds  external  vent. 

In  long-established  cases  deposits  of  pus  calculi  (serumal)  may 
form  upon  the  root  end  (Fig.  441).  'i'he  cement  corpuscles  of  the 
a}>ical  c-enientum  may  die  and  the  root  tissue  itself  become  infected, 
in  otiier  cases  resorption  of  the  root  cud  occurs.     (See  Resorption.) 

Symptoms. — In  all  of  these  cases  the  formations  are  gradual,  owing 
to  the  partial  vent,  and  it  may  be  that  no  pain  beyond  a  slight  gnaw- 
ing or  feeling  of  fulness  or  an  occasional  reflex  pain  may  occur.     If 


CHRONIC  APICAL  ABSCfiSS 


537 


for  any  reason  the  vent  become  occhuled,  the  ])U,s  formation  becomes 
rapid  and  an  acute  abscess  is  set  up,  which  may  be  painful  or  not, 
according  to  the  amount  of  tension  produced  before  (h'scharge  of  the 
pus.    Aside  from  tliis,  the  gum  color  at  the  apex  is  sonunx  hat  deepened, 


Fig.  438 


Fig.  430 


Chronic    blind    abscess    upon    lower 
Chronic  blind  abscess  of  upper  incisor,  sliowing      tooth,  showing   tendency  of  pus   to  sink 
tendency  of  pus  to  progressively    destroy    perice-      into  the  substance  of  the  lower  maxilla, 
nientum,  owing  to  the  influence  of  gravity.  (jwing  to  the  influence  of  gravity. 


Fig.  440 


Fig.  441 


Chronic  apical  abscess  discharging  through  Chronic   abscess,    showing    denudation    of 

the  hard  palate  and  tlireatening  to  discharge       apex  of  root  (a  to  6),  with  deposits  of  calculi 
labially.  (a)  upon  cenientuin. 


the  tooth  is  .slightly  loosened,  and  slightly  tender  to  percussion.  Signs 
of  previous  moist  gangrene  are  in  evidence. 

Diagnosis. — The  passage,  without  production  of  sen.sation,  of  an 
undue  length  of  fine  probe  into  a  canal  is  evidence  of  destruction  of 
apical  tissue  and  a  guide  to  its  probable  extent. 

An  extensively  inflamed  gum  tissue  over  the  apex  indicates  a  prob- 


538  DISEASES^  OF  THE  PERICEMENTUM 

able  approach  of  pus  formation  to  gum  tissue.  The  presence  of  pus 
in  the  canal  or  upon  several  dry  cottons  introduced  for  absorbent 
purposes  is  diagnostic.  If  pus  be  not  seen,  and  the  canal  be  thor- 
oughly sterilized  and  dressed  with  an  antiseptic,  the  supervention  of  an 
acute  abscess  affords  evidence  of  the  presence  of  an  abscess  sac  or 
cavity.     The  a'-rays  afford  a  means  of  diagnosis  (Fig.  430), 

Prognosis. — The  prognosis  is  favorable  to  a  cure  in  nearly  all  of 
these  cases,  provided  thorough  canal  asepsis  and  filling  can  be  attained 
and  the  abscess  cavity  can  be  drained  and  disinfected.  In  cases 
resisting  this  treatment,  a  fistula  must  be  established. 

Treatment. — ^The  first  and  second  grades  of  chronic  apical  abscess 
discharging  via  the  canal  may  be  treated  upon  exactly  the  same 
principles  which  are  involved  in  the  treatment  of  moist  gangrene 
of  the  pulp.  The  infection  is  considered  as  simply  more  deep  seated, 
so  that  it  is  necessary  to  pass  disinfectants  into  the  abscess  cavity 
with  two  objects  in  view:  (1)  to  destroy  the  bacteria  present;  (2)  to 
stimulate  the  tissues  to  granulative  activity.  To  accomplish  this  the 
apical  foramen  must  be  opened.  The  canal  should  be  sterilized  with 
sodium  dioxide  and  the  foramen  very  slightly  enlarged  with  a  fine 
Donaldson  cleanser,  the  canal  having  been  flooded  with  5  per  cent, 
formalin  as  an  antiseptic. 

If  necessary  the  root  canal  may  be  otherwise  enlarged.     (See  p.  482. ) 

A  dressing  of  10  per  cent,  formalin  or  phenol  camphor  to  which  a 
little  menthol  and  a  drop  of  formaldehyde,  40  per  cent.,  has  been  added, 
or  tricresol  and  formaldehyde,  equal  parts,  should  be  loosely  placed  in 
the  canal  and  the  tooth  sealed  for  twenty-four  hours,  or,  if  the  tooth 
has  been  very  troublesome  and  still  tender,  a  soft  temporary  stopping 
may  be  used  and  the  patient  provided  with  instruments  suited  to  the 
removal  of  the  covering  and  the  cotton.  It  is  better  that  the  tooth 
should  be  under  the  control  of  the  patient.  At  the  next  sitting  the 
stoppings  are  more  tighdy  made.  The  Zierler-Hoffendahl  method 
may  be  used  to  sterilize  the  root  and  abscess,  then  the  dressing  is 
sealed  in  for  a  few  days  (p.  504).  When  no  pus  can  be  found  on 
the  dressing  or  following  it,  or  on  an  exploratory  cotton  twist,  and 
there  is  no  odor,  the  root  may  be  filled;  in  case  of  any  doubt  in  fine 
roots,  with  a  removable  material  such  as  forma-percha  on  cotton  or 
the  paraform  alum  paste  (p.  488),  which  may  remain  if  no  ill-results 
follow.  A  temporary  crown  filling  of  gutta-percha  should  be  used  for 
a  week  or  two.  Each  change  of  dressing  should  be  prec(>ded  by 
sterilization  of  the  cavity  and  bulb  of  the  pulp  cliiunber  with  a  strong 


CHRONIC  APICAL  ABSCESS  539 

formalin  solution  to  prevent  re-infection  of  the  apical  tissue  durint^ 
the  change,  and  it  is  well  to  use  counterirritation  directly  after  the 
root  filling. 

It  is  always  well  when  using  an  occlusal  opening  to  close  it  with 
amalgam  or  cement,  while  compressible  dressings  are  in  place,  as 
even  one  heavy  bite  upon  the  covering  may  force  the  medicament 
into  the  apical  tissue  and  renew  the  irritation.  Slightly  counter- 
sinking the  orifice  of  the  tap  will  prevent  an  inward  thrust  of  a  rigid 
covering  overlying  cotton. 

Some  operators  prefer  to  leave  a  small  vent  in  the  temporary 
covering,  used  to  act  as  a  drain.  This,  however,  is  apt  to  prevent 
the  concentration  of  the  action  of  the  medicament  upon  the  apical 
tissue. 

If  pus  formation  persist  in  any  case,  and  especially  if  no  pain  has 
been  produced,  good  results  sometimes  follow  a  departure  to  the 
immediate  method  of  root  filling.  The  canal  and  pus  cavity  are 
re-sterilized,  a  little  zinc  chloride  or  carbolic  acid  is  pressed  into  the 
apical  tissue,  and  the  canal  apex  filled  with  gutta-percha  or  oxychloride 
of  zinc.  The  tissues  are  expected  to  care  for  themselves.  A  persistent 
discharge  of  serum  or  glairy  lymph  are  indicative  of  inflamed  aseptic 
but  weeping  tissue,  and  require  the  same  treatment.     (See  p.  485.) 

Cyst  formation  occurs  owing  to  the  projection  of  an  aseptic  root 
filling  or  to  some  not  well-understood  cause;  a  cystic  swelling  may 
occur  over  the  root  of  a  tooth  and  have  its  origin  in  the  pericementum. 
Usually  the  cause  is  not  septic,  otherwise  it  has  the  characteristics  of 
pericemental  or  apical  abscess.  The  swelling  is  apt  to  be  bluish 
about  its  margin,  and  has  a  clear  stretched  look  in  the  centre.  It 
is  probably  due  to  a  collection  of  fluid  in  some  portion  of  the  peri- 
cementum, or  may  have  as  its  excitant  a  portion  of  calculus  deposited 
aseptically  in  the  pericementum.  Indeed,  apart  from  infection,  it  may 
be  that  cases  of  pericemental  abscess  cases,  discharging  merely  glairy 
fluid,  are  cystic  swellings. 

If,  on  the  other  hand,  pus  formation  increase  or  be  persistent,  an 
artificial  fistula  must  be  established  (see  p.  528)  and  the  case  tn>ated 
as  a  chronic  apical  abscess  with  fistula. 

In  the  third  and  fourth  grades  the  prognosis  for  treatment  by  way 
of  the  canal  is  not,  as  a  rule,  good,  but  if  desired  may  be  attempted. 
If,  however,  an  artificial  fistula  be  established,  the  ease  of  treatment  is 
greatly  increased.  The  case  is  then  treated  as  a  chronic  apical  abscess 
with  fistula. 


540  DISEASES  OF   THE  PERICEMEXTUM 

In  no  case  should  hydrogen  dioxide  be  forced  in  quantity  into  the 
pus  occupying  such  an  abscess  cavity  until  the  fistula  has  been  made, 
and  it  is  better  even  then  that  the  bulk  of  it  be  washed  out  with  warm 
water  before  applying  the  drug.  A  neglect  of  this  precaution  may 
bring  about  great  pain,  owing  to  the  rapid  reaction  of  the  hydrogen 
dioxide  with  the  pus  and  blood  present. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA. 

Morbid  Anatomy  and  Pathology. — ^This  form  of  chronic  abscess 
occurs  as  the  result  of  the  discharge  of  an  acute  abscess  through  the 
gum  or  other  part  to  the  surface  of  the  body.  (The  interior  of  the 
mouth  or  other  cavity  exposed  to  contact  with  the  air  is  considered 
external  to  the  body  proper  and  whether  the  fistula  has  naturally 
occurred  or  been  artificially  established.) 

If  the  acute  abscess  has  been  severe  or  long  continued,  the  tissue 
destruction  may  be  great,  but,  as  a  rule,  granulation  promptly  sets 
in  and  the  walls  of  the  abscess  cavity  organize  into  cicatricial  tissue. 
From  the  interior  of  this  a  canal  (fistula)  lined  with  cicatricial  tissue 
leads  to  the  surface,  the  pus  being  almost  constantly  formed  at  the 
expense  of  the  granulation  tissue  which  is  as  constantly  renewed. 

The  fistulous  opening,  as  a  rule,  appears  as  a  small  teat  of  inflamed 
tissue  located  in  the  majority  of  cases  upon  the  buccal  surface  of  the 
gum,  about  a  quarter  of  an  inch  below  the  apex  of  the  root  and  slightly 
distal  to  it — a  position  probably  determined  by  the  density  of  the 
tissues  surrounding  the  acute  abscess.  At  times  the  only  evidence  of 
a  fistula  is  a  small  spot  of  inflammation  surrounding  a  minute  opening 
from  which  pus  exudes.  The  fistula  is  sometimes  located  upon  the 
lingual  surface  of  the  gum.  It  may  perforate  the  bone  of  the  hard 
palate  and  open  through  the  mucous  membrane  of  the  roof  of  the 
mouth  (Fig.  440).  Instead  of  finding  exit  by  a  direct  path  through 
the  buccal  or  lingual  alveolar  plate  and  gum,  the  pus  may  burrow 
along  the  length  of  the  pericementum  and  discharge  at  the  neck  of 
the  tooth  (Figs.  426  and  427).  One-half  or  more  of  the  lateral  aspect 
of  the  pericementum  may  remain  vital,  although  involved  in  a  chronic 
inflammation,  the  remainder  being  destroyed.  Not  infrequently  the 
pus  burrows  along  the  surface  of  the  bone  and  discharges  at  a  point 
over  an  edentulous  portion  of  the  jaw.  This  is  common  to  a  lower 
bicuspid. 


CHROXIC  APICAL  AH.SCESS  WITH   FISTULA 


541 


Where  the  apices  of  the  roots  of  upper  posterior  teeth  He  in  very  close 
proximity  to  the  floor  of  the  antrum,  perforation  of  this  floor  may  occur 
before  tissue  destruction  has  proceeded  far  enough  in  other  (hrections 
to  afford  escape  to  the  pus  (Fig.  429).  Extensive  pus  accumu- 
lations may  occur  in  the  antrum  in  consequence.  It  may  dis- 
charge into  the  nasal  cavity,  in  connection  with  acute  abscess;  at  such 
points  the  discharge  may  remain  persistent.     Sometimes  the  discharge 


Fig.   442 


Fig.  443 


Chronic  apical  abscess  on  mesial  root. 
Ultimate  result  of  a  pulp  capping.  Editor's 
practice.     (Skiagraph  by  Hagopian.) 


occurs  through  the  canal  of  the 
affected  tooth ;  the  condition  then 
becomes  one  of  blind  abscess 
(Fig.  422).  Upon  a  lower  tooth, 
particularly  the  incisors,  the  pus 
may  burrow  downward  through 
the  cancellated  tissue  of  the  bone 
and  emerge  at  the  base  of  the 
bone  and  open  upon  the  face 
(Figs.,443and44o). 

In  other  ca.ses  the  pus  may  per- 
forate the  bone  and  find  passage 

along  the  submuscular  tissue,  opening  uj^on  the  face  or  neck  (Fig. 
445).  The  apices  of  the  roots  of  teeth  lying  beneath  the  line  of 
insertion  of  the  mylohyoid  muscle  may  cause  an  ab.scess  to  oj)en  in  the 
neck  cavity.  Cryer  records  a  case  where  an  abscess  openitig  upon  the 
face  immediately  anterior  to  the  line  of  the  facial  artery  was  trac(>d  to 
the  root  of  a  lower  molar;  the  direction  of  the  sinus  is  shown  in 
Fig.  446.  In  a  case  having  a  similar  anatomical  association  the  pus 
penetrated  the  bone  lingually,  was  encap.suled  beneath  tlic  internal 
pterygoid  muscle,  and  appeared  as  a  swelling  at  the  inner  aspect  of 


Cliroiiio  alveohir  abscess  of  the  root  of  the 
lower  incisor,  with  abscess  cavity  passing 
through  the  body  of  tlie  bone  and  discharging 
on  the  skin  beneath  tlie  chin:  n,  very  large 
abscess  cavity;  6,  mouth  of  the  fistula. 
(Black.) 


542 


DISEASES  OF  THE  PERICEMENTUM 


the  angle  of  the  jaw.  Occasionally  the  apices  of  the  roots  of  lower 
molars  are  separated  from  the  inferior  dental  canal  by  only  a  thin 
lamina  of  bone,  so  that  discharge  into  this  canal  may  occur  with 
infiltration  along  the  vessels  and  nerves  iniTthe'^canaiy(Fig.   220). 


Fig.  444 


Fig.   445 


Fistula  passing  down  through  the  body  of  the  lower 
maxilla.     (Black.) 


While  discharge  into,  the  nasal  chamber 
is  most  frequently  associated  with  ab- 
scess upon  the  central  incisors, 
abscesses  upon  molars  may  discharge 
into  the  same  cavity. 

Cementum    infection    occurs    as    a 

Chronic  alveolar  abscess  at  the  root  of 
sequence   to   death   of    the    cement  cor-    a  lower  incisor,  with   a  fistula   discharg- 

puscles  from  lack  of  nutrition.     Pus 


ing  on   the  face  under  the  chin:  a,  ab- 
scess cavity  in  the  bone;  b,  b,  b,  fistula 
calculi    may   also   form  on    the    roots   in    following  in  the  periosteum  down  to  the 
,       ,  .  ,  ^P,,  lower  margin  of  the  body  of  the  bone  and 

the  long-contmued  cases.      1  he  granu-  discharging  on  the  skin.    (Black.) 
lation   tissue  springing  up  about  the 

parts  has  a  resorbent  action  and  the  root  ends  are  often  resorbed, 
though  this  action  is  probably  to  an  extent  counteracted  by  the  alka- 
linity of  the  pus.  The  formation  of  the  latter  may,  however,  be  in 
abeyance  at  times  (Fig.  448). 

The  extent  of  ti.ssue  destruction  varies  considerably,  but  is  usually 
greatest  in  dependent  parts,  gravity  influencing  the  burrowing  of  the 
pus. 

Symptoms  and  Diagnosis. — A  fistula  is  seen  upon  the  gum,  visible  as 
either  a  small  teat  of  flesh  (perhaps  pedunculated),  discharging  pus, 
or  as  a  tiny  orifice  in  the  gum  surrounded  by  inflamed  tissue,  and 
from  wliich  pus  may  be  squeezed  (Fig.  428).  As  a  rule,  a  soft  silver 
probe  may  be  passed  to  the  apex  of  a  nearby  root,  whether  possessing 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA 


543 


a  crown  or  embedded  in  the  bone.     In  case  of  an  external  ojjcning 
upon  tlic  face  a  similar  procedure  shows  the  troul)le  to  lie  with  some 


Fig.   446 


Fig.   447 


Fig.  448 


Abscess  with  tortuous  sinus,  opening 
upon  the  face:  A,  tissue  of  cheek;  B, 
floor  of  mouth;  C,  abscess  tract. 

tooth  root.  The  .r-rays  will 
sometimes  be  valuable  in  de- 
termiiiino'  the  exact  location  of 

tne  abscess  cavity.  Large  abscess  cavity  in  relation  with  a  lateral 

Upon    the    teeth     themselves  incisor,    complicated    by    an    impacted    supernu- 

,   .  merary  tooth  beneath  the  nasal  spine.     (Phila- 

but  four  conditions  may  cause  delphia  Dental  College  Museum.) 

a  fistulous  opening:  (1)  moist 

gangrene  of  the  pulp  or  its  equivalent  apical  infection;  sometimes 

the  sinus  is  at  the  oral  end  of  a  broken  root;   (2)  septic  perforations, 

apical  or  lateral;  (3)  a  pericemental  abscess 

(see  Pericemental  Abscess);  (4)  a  secondary 

abscess  associated  with  a  pyorrhea  pocket. 

(See  Pyorrhea  Alveolaris.) 

Aside  from  these,  the  probe  may  lead  to 
carious  or  necro.sed  bone,  a  cyst,  an  im- 
pacted tooth,  or  a  subperiosteal  abscess 
(maxillary  periostitis). 

In  these  cases  the  probe  does  not  lead 
to  a  root.  Carious  bone  will  im[)art  a 
honey -combed  sensation  to  an  excavator; 
necro.sed  bone  will  be  exposed  and  firm, 
or  the  .sequestruni  will  be  in  evidence  as  a 
movable  body.  There  may  also  be  several 
fistulas  and  extensive  inflammation  of  the 

tissue.     Aeyst  will  be  a  tumor  with  certain  characteristics,  and  an  im- 
pacted tooth  will  usually  impart  the  feel  of  smooth  enamel   to  the 


.\bscess  and  resorption  at  apex. 
(Skiagraph  by  Lodge.) 


544  DISEASES  OF  THE  PERICEMENTUM 

instrument,  though  the  enamel  may  at  times  be  rough  at  certain 
points.  An  embedded  root  will  be  movable,  and  will  present 
the  dentine  and  its  central  opening,  the  pulp  canal,  as  diagnostic 
features.  Maxillary  periostitis  will,  as  a  rule,  have  a  history  of 
traumatism,  or  the  previous  use  of  a  probably  infected  hypodermic 
needle^  associated  with  it.  In  all  cases  not  clearly  due  to  other  than 
dental  causes,  evidence  of  the  four  dental  conditions  mentioned  should 
be  sought. 

Treatment. — In  cases  arising  from  sources  not  dental,  surgical  inter- 
ference for  the  removal  of  the  cause  is  necessary.  This  may  require 
a  minor  or  major  operation,  according  to  the  case. 

In  the  purely  dental  cases  the  cause  must  also  be  removed.  If 
due  to  pericemental  abscess,  this  is  to  be  treated.  If  due  to  a  septic 
perforation  not  yielding  to  treatment  by  way  of  the  root  canal, 
the  fistula  may  be  enlarged,  packed  open  with  antiseptic  cotton  or 
gauze  applied  on  successive  days,  and  when  the  perforation  is  exposed 
it  may  be  filled  with  amalgam.  If  properly  done  the  fistula  should 
heal.  If  this  operation  be  impossible,  the  root  should  be  amputated 
at  a  point  between  the  perforation  and  the  crown.  If  the  perforation 
be  in  the  middle  or  cervical  third  of  the  root,  it  may  at  times  be  treated 
from  the  root  canal.  A  good  method  is  to  force  root-filling  material 
through  the  perforation  and  fistula  and  to  smooth  it  off  through 
the  sinus.  Stiff  oxychloride  of  zinc  or  oxyphosphite  of  copper  are 
excellent.  If  incurable,  the  entire  root  must  be  amputated  in  case  of 
a  multi-rooted  tooth.  In  case  of  a  single-rooted  tooth  the  tooth  must 
be  extracted,  and  if  the  conditions  warrant  the  operation  the  root 
may  be  perfectly  sterilized,  properly  filled,  and  then  replanted  after 
the  associated  abscess  cavity  has  been  surgically  obliterated. 

In  the  cases  due  to  moist  gangrene  of  the  pulp  the  canals  must  be 
freely  entered,  the  apical  foramen  opened  with  Donaldson  or  other 
cleansers,  and  the  canals  and  abscess  tract  thoroughly  sterilized. 

The  canals  are  sterilized  with  sodium  dioxide  freely  used.  The 
canal  is  flooded  with  3  per  cent,  hydrogen  dioxide,  and  with  a  Swiss 
broach  upon  which  cotton  is  wound  a  plunging  force  is  exerted  upon 
the  fluid  in  the  canal.  This  tends  to  drive  it  into  the  abscess  cavity 
and  out  of  the  fistula,  flushing  and  sterilizing  the  abscess  tract.  This 
is  then  repeated.  If  this  simple  procedure  be  not  effective,  a  thread 
of  cotton  saturated  with  hydrogen  dioxide  should  be  placed  in  the 
canal.     Pressure   is   tlien   exerted   witli    vulcanizablc   rubber,   as   in 

'  Boeiining,  Dental  Cosmos,  1902. 


CilUOXIC   Al'ICAL   ABSCKSS    WITH    FISTULA 


545 


pressure  anesthesia.  A  third  method  eonsists  of  filhn^  the  erowii 
cavity  with  lijutta-pereha  or  vulcanite  rubber,  for(in«i-  the  nozzle  of 
an  abscess  s_vrin(i:;e  throu<;h  the  mass,  and  drivintj:  down  the  piston  of 
the  syrint,^e.     In  all  these  procedures,  except  the  initial  sterilization, 


Minim   syiiiige. 


Fig.  450 


.1.    N.    Fairar's  ahoolar-aliM-css  syiintio. 


the  unart'ected  roots  of  multi-rooted  teeth  are  to  be  avoided  so  far  as 
possible,  as  undue  pressure  may  excite  an  abscess.  The  fistula  will 
admit  the  nozzle  of  the  syringe,  which  may  be  used  to  flush  out  the 
abscess  tract  with  hydroijen  dioxide. 

The  nozzle  of  a  hypodermic  needle  may  be  htted  to  the  canal  by 
35 


546  DISEASES  OF  THE  PERICEMENTUM 

packing  wax,  temporary  stopping,  or  raw  vulcanite  about  it;  a  piece  of 
flexible  tubing  may  be  previously  stretched  over  the  free  end  and  later 
the  other  end  of  the  tubing  stripped  over  the  compressed-air  syringe. 
INIedicaments  or  air  may  thus  be  blown  through  the  fistula.  The 
method  should  be  cautiously  used  in  fistulous  cases  only,  except  for 
reasons  well  known  by  the  operator  employing  them,  as  very  painful 
distention  and  even  emphysema  of  the  cheek  may  occur.  (See  Index.) 
All  preliminary  work  having  been  done  as  well  as  possible, 
tricresol  and  formalin  are  to  be  pumped  into  the  abscess  tract  and 
the  canal  temporarily  stopped  with  the  same  antiseptic  on  cotton. 
With  this  treatment  the  discharge  of  pus  should  cease  and  be 
replaced  by  serum.  It  is  good  practice  to  re-sterilize  the  canal 
and  fill  it  as  soon  as  this  result  is  noted,  or,  in  emergency  cases, 
the  canal  may  be  filled  at  the  first  sitting  after  prolonged  germicidal 
work.     The  fistula  then  will  probably  heal  uninterruptedly  in  the 

Fig.  451 


Bulb  syringe. 

vast  majority  of  cases.  In  a  week  or  two  the  fistula  should  have 
healed  if  attached  to  treatable  canals;  for  the  difficult  canals  sub- 
jected to  germicides  only  more  time  may  be  required,  but  healing 
usually  eventually  occurs  owing  to  the  removal  of  the  cause. 

If  the  abscess  cavity  does  not  heal,  one  of  several  causes  may 
be  assigned:  (1)  the  crypts  in  the  walls  of  the  abscess  cavity  may 
require  further  disinfection;  (2)  the  cotton  in  the  canal  may  have 
absorbed  pus  formed  after  an  interval  of  antiseptic  influence  and  may 
keep  up  the  infection;  (3)  the  root  canal  may  not  be  explorable;  (4) 
the  root  end  may  Ik;  incrusted  with  calculus,  or  the  cementum  be 
infected,  or  dead  l)on(!  may  be  present. 

For  the  first  (;ondition  the  canal  and  abscess  tract  may  be  treated 
with  10  percent,  zinc  chloride,  or  mercuric  chloride  maybe  added  to 
hydrogen  (h'oxide  (1  to  500  or  1  to  1000)  and  the  abscess  cavity  syringed 
out  at  intervals.     For  the  second  condition  a  non-absorbent  dressing 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  547 

slunilcl  he  used,  such  us  fornia-pcrcha,  or  the  root  apex  may  be  perma- 
nently filled  with  gutta-percha.  In  the  fine,  unexplorable  canals 
25  per  cent,  pyrozone  may  be  used  for  twenty-four  hours,  as  though 
bleaching  the  root,  or  Rhein's  cataphoric  method  (see  p.  485)  may  be 
employed.  In  some  cases  abscesses  require  some  weeks  to  heal,  but 
eventually  do  so,  particularly  if  the  abscess  be  syringed  out  with  an 
antiseptic  every  third  day  via  the  fistula. 

Tissues  about  abscesses  have  an  inherent  tendency  to  regeneration; 
cases  of  long  standing  frequently  healing  promptly,  sometimes,  though 
not  often,  in  twenty-four  hours.^ 

In  indolent  chronic  inflammation  the  use  of  a  small  gum  dry  cup 
with  vacuum  bulb  attached  may  be  used  for  five  or  ten  minutes  at  a 
time  for  an  hour  or  so,  to  draw  fresh  blood  and  effusions  into  the 
inflamed  part.  The  opsonic  index  of  the 
lymph  drawn  in  is  said  to  be  raised  to 
several  times  beyond  that  of  the  body 
lymph,  thus  rapidly  increasing  phagocy- 
tosis in  the  part. 

For  the  fourth  class  of  cases  the  apical 
foramen  should  be  sealed  and  the  abscess 
tract  syringed  once  a  week  with  25  per 
cent,  sulphuric  acid,  the  mouth  and  cloth- 
ing being  properly  protected  by  using  a        Amputation  of  root  apex:  oa. 

<~ixi^./i  ./  o  opening    in    the  gum    made    by 

pad     of    COttonoid     over     the     fistula     and       packing  fistula;  AC,  abscess  cav- 

needle  to  absorb  the  excess.  This  dis-  ity; /?f,  root  filling. 
solves  calculi  and  disinfects  dead  ceraentum.  It  also  stimulates 
the  soft  parts  to  a  granulative  action.  If  necessary  the  patient  should 
receive  appropriate  systemic  treatment,  especially  if  anemic.  (See 
p.  97.)  In  this  way  some  old  and  somewhat  obstinate  cases  may 
be  induced  to  heal.  Many  apparently  desperate  cases  heal  of  their 
own  accord  after  some  months.  Some  success  attends  the  packing 
of  a  root  with  a  thick  paste  of  iodoform  in  any  oil  after  opening  th(> 
root  as  far  as  possible.  Cases  in  which  a  canal  was  not  explorabU' 
for  any  considerable  distance  have  healed  after  this  treatment.  The 
x-ray  application,  made  for  ten  or  twenty  seconds,  or  skiagraphy  seems 
to  aid  the  healing  of  the  fistula.  If  the  abscess  be  incurable  by  the 
above  method,  or  radical  measures  being  considered  better,  the  root 
end  may  be  amputated.  The  fistula  is  enlarged  and  packed  open 
with  antiseptic  gauze  or  cotton  and  sandarac  varnish  dipped  into 

•  Darby,  Proceedings  Academy  of  Stomatology,  Philadelphia,  1899. 


548 


DISEASES  OF  THE  PERICEMENTUM 


powdered  orthoform  applied  until  the  root  end  is  fairly  in  view.  After 
sterilization  of  the  abscess  cavity  and  local  anesthesia,  a  dentate  fissure 
bur  or  a  Schamburg  surgical  bur  is  laid  upon  one  side  of  the  root 
at  the  level  of  the  healthy  tissue,  and  carried  laterally  with  a  sawing 
motion  until  the  root  end  is  separated.  It  may  readily  be  picked  out. 
If  the  root  can  be  correctly  located  without  packing  the  fistula  the 
part  may  be  anesthetized  and  a  portion  of  gum  may  be  cut  away 
with  a  tubular  knife,  or  an  incision  may  be  made,  after  which  a 
fissure  or  surgical  bur  may  be  used  to  cut  away  the  root.  iVny 
necrosed  bone  may  be  removed  at  the  same  time.  A  skiagraph  to 
act  as  a  guide  is  necessary  when  the  fistula  is  not  packed  open. 


Fig.  453 


Fig.  454 


Fig.  455 


A  skiagraph  of  apical  abscess 
cavity  about  two  root  apices; 
incurable  by  ordinary  means. 


The  same  after  root  ampu- 
tation. 


The  same  thirty  days 
later,  showing  a  certain 
amount  of  new  bone  for- 
mation.     (Price.) 


Necrosed  root  ends  may  occasionally  be  seen  projecting  through  the 
gum  and  alveolar  process  which  have  been  lost  above  them.  They 
should  be  removed  as  above  indicated.  Sometimes  salivary  calculus 
deposits  on  them. 

Anti.septic  gauze  should  be  packed  into  the  abscess  cavity 
after  operation  to  stimulate  granulation.  The  quantity  of  gauze 
should  l)e  gradually  lessened  until  the  cavity  is  nearly  healed.  It 
should  thereafter  be  kept  sterilized  by  means  of  hydrogen  dioxide 
until  the  cavity  has  healed.  Stimulation  by  means  of  fused  silver 
nitrate  or  sulphuric  acid  or  scarification  is  at  times  necessary.  Bone 
should  gradually  be  deposited  about  the  roots  (Figs.  453,  454,  and 
455).  Failure  indicates  some  condition  of  .sepsis;  presumably  the 
amputation  has  not  included  all  septic  root  or  the  canal  filling  is 
defective. 

A  still   more   radical   method   of  surgical   treatment  involves   the 


CHRONIC  A  PIC  A  J.  ABSCESS  WIT  If  FISTULA  o-lO 

extraction  and  replantation  of  tiic  root.  'I'lic  mouth  is  .sterilized  and 
the  tooth  extracted,  care  being  taken  not  to  injure  the  enamel  with  the 
forceps.  It  is  then  placed  in  a  1  to  1000  solution  of  mercuric  chloride 
at  120°  F.  The  apex  of  the  alveolus  is  in  the  meantime  sterilized 
with  hydrogen  dioxide  plus  mercuric  chloride  and  thoroughly  curetted. 
Bleeding  is  checked  with  the  same  solution  or  atlrenalin  chloride,  and 
a  tampon  of  cotton  saturated  with  a  20  per  cent,  solution  of  phenol- 
sodique  is  packed  into  the  alveolus. 

Returning  to  the  tooth,  the  apex  is  cut  off  slightly  beyond  the  denuded 
area  and  smoothed;  the  pulp  canal  is  well  opened  from  the  apex,  all 
(lel)ris  removed  from  it,  and  it  is  then  well  sterilized  with  sodium 
dioxide  or  25  per  cent,  pyrozone,  or  both.  The  canal  is  then  dried 
and  filled  entirely  with  gutta-percha,  or  {)artly  with  gutta-percha  and 
the  operation  completed  with  gold,  which  is  nicely  smoothed.  The 
root  should  be  handled  in  an  aseptic  napkin  or  one  wet  with  the  anti- 
septic, and  when  ready  should  be  returned  to  the  sterilizing  solution. 
All  being  ready,  the  tampon  is  removed,  the  tooth  replaced  in  its  socket, 
and  a  previously  prepared  retaining  appliance  cemented  to  place. 
This  should  remain  from  three  to  six  weeks  and  be  replaced  shoidd 
indications  demand  it.  If  the  tooth  be  valueless  for  replantation 
purposes,  the  operation  of  transplantation  may  be  done  either  imme- 
diately after  extraction  of  the  offending  tooth  or  a  few  days  later. 
The  possibility  of  resorption  of  the  root  after  plantations  should  have 
careful  consideration,  though  it  is  not  prohibitory. 

The  operation  of  transplantation  may  be  done  with  a  tooth  recently 
extracted  from  another  mouth  or  with  a  dried  tooth,  or,  preferably, 
teeth  kept  in  alcohol  and  glycerin,  which  many  extracting  specialists 
habitually  retain  to  oblige  applicants.  If  a  suitable  tooth  be  not  ol)tain- 
able,  the  root  may  have  a  crown  mounted  upon  it  in  such  manner  as 
to  have  an  open  joint  at  a  point  to  be  placed  beneath  the  gum  line, 
and  this  joint  slioukl  be  filled  with  cohesive  gold  and  })()lished.  The 
tooth  root  is,  of  course,  sterilized  previous  to  and  after  the  crown 
mounting,  and  its  canal  shoukl  have  been  thoroughly  filled  with  gutta- 
percha. Any  of  these  may  become  firm  if  thoroughly  splinted  for  a 
proper  length  of  time.  The  alveolus  shoukl  be  made  to  fit  the  root 
snugly  by  means  of  a  bone  reamer.  The  operation  of  im])lantation 
differs  from  this  oidy  in  the  fact  that  it  is  done  where  a  tootii  alv(olus 
has  been  obliterated  by  absorption  and  bone  formation,  as  after 
extraction.  If  the  tooth  be  not  lost  by  resorption,  it  is  probable  that 
some  resorption  occurs — toleration  then  ensues  and  bony  deposition 


550  DISEASES  OF  THE  PERICEMENTUM 

in  the  bays  of  resorption  and  about  the  root  occurs.  Possibly  a  true 
ankylosis  (which  see)  may  occur. 

To  select  a  proper  tooth  make  a  model  and  bite  from  an  impression 
taken  before  extraction  or  immediately  thereafter,  cut  off  the  offending 
tooth  from  the  model,  ream  out  a  socket  in  the  plaster;  select  tooth,  and 
fit  in  place;  attach  with  a  little  soft  piaster,  the  model  being  thoroughly 
wet.  Construct  the  retaining  appliance,  remove  the  tooth,  sterilize,  and 
fill  the  root.  Then  put  the  tooth  in  the  sterilizing  agent  until  needed. 
Mendel-Joseph  and  Dassonville^  have  shown  that  in  case  of  removal 
of  a  portion  of  the  pericementum  the  lost  portion  may  be  regenerated. 

Several  cases  of  fistulous  openings  into  the  antrum  have  been  noted 
by  canal  exploration  in  which  no  history  of  discomfo/t  from  antral 
empyema  could  be  obtained.  It  was  assumed  that  the  root  ends 
approximated  the  floor  of  the  antrum,  and  that  the  abscesses  were 
of  simple  chronic  type.  Such  cases  were  treated  upon  the  common 
principle  of  canal  antisepsis,  flushing  the  abscess  tract  with  hydrogen 
dioxide,  and  filling  the  canals,  though  simple  non-eff'ervescing  solutions 
are  better.  The  antral  condition  was  explained  to  the  patients,  who 
were  warned  of  possibilities,  but  such  as  yet  have  not  been  reported. 

A  chronic  abscess  may  discharge  into  the  maxillary  sinus  for  a 
long  period  before  being  discovered,  unless  the  pus  accumulation  be 
extensive,  when  it  escapes  from  the  antrum  into  the  cavity  of  the  nose, 
discharging  by  one  side.  Smaller  accumulations  of  pus  find  exit  in 
the  recumbent  position,  and  attention  is  called  to  one  antrum  as  the 
seat  of  affection  by  noting  that  in  the  morning  pus  appears  at  but  one 
nostril.  The  discharges  from  purulent  nasal  catarrh  appear  upon 
both  sides. 

A  more  common  history  of  antral  empyema  is  the  patient's  com- 
plaint of  dull,  heavy  pains  and  uneasiness  over  one  side  of  the  face, 
and  an  offensive  odor,  which  may  not  be  evident  to  the  operator. 
High  transillumination  of  the  tissues  about  the  mouth  and  through 
the  cheek,  by  means  of  the  electric  mouth  lamp  of  20  volts  capacity, 
the  patient  being  in  a  dark  room,  may  reveal  an  opacity  on  one  or 
perhaps  both  sides,  indicating  the  presence  of  fluid  in  the  antrum.  A 
clear  pinkish  transillumination  is  a  sign  of  health.  Tumors  in  tlic 
antrum  entirely  obstruct  the  light.  Examination  of  the  posterior  teeth 
will  show  one  of  them  to  be  pulpless,  if  the  cause  lie  in  apical  abscess. 
If  such  a  tooth  be  extracted  a  profuse  flow  of  pus  may  follow,  and  a 
probe  may  Ik;  passed  through  an  alveolus  directly  into  the  antrum. 

>  Dental  Cosmos,  lOOf.,  p.  10.59. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  551 

It  is  to  be  rcmembeivd  that  antral  empyema  may  occur  from  the 
influenza  bacillus  in  the  blood.  It  has  been  noted  in  connection  with 
la  grifpe  and  may  be  secondary  to  empyema  of  the  other  sinuses. 
The  aj-rays  are  valuable  diagnostic  means  (Fig.  456). 

The  shadow  of  the  affected  side  is  due  to  pus  or  even  to  thickened 
walls  and  increased  vascularity.  Skiagraphy  either  through  the 
alveolar  process  or  anteroposteriorly  through  the  heatl  ex])oses  the 
various  possible  causes,  the  condition  of  the  teeth,  or,  in  the  antero- 
posterior, a  possible  ethmoiditis  or  frontal  sinusitis  may  be  diagnosti- 
cated as  the  primary  cause,  or  as  a  condition  secondary  to  a  primary 
antral  suppuration. 

Although  extraction  is  the  usual  surgical  relief,  dental  conservatism 
rebels  against  the  immediate   condemnation  of  the  offending  tooth. 
Efforts  at  curing  the  antral  con- 
dition through  the  pulp  canal  are  Fig.  456 
well-nigh  hopeless — the  antrum  is 
entereti  at  some  other  point.    The 
tooth  is  treated  as  any  infecting 
root;  is  sterilized  and  filled.     The 
most  certain  spot  of  entry  to  the 
antrum  is  about  one-<]uarter  inch 
above  the    buccal    roots    of    the 
upper  first  molar  or  between  the 
roots  of    the    first    and    second 

molar.      The   part,  or  the  patient,  Empyema  of  antrum  due  to  abscess  upon 

,       .  ,  .      .  root   of   biscuspid    tooth.      (Radiograph  by 

IS  anesthetized  and  the  soft  tissues     price.) 
incised   or  a  section  removed  by 

means  of  a  tubular  knife;  a  drill  or  trephine  at  least  one-eighth  inch 
in  diameter,  driven  rapidly,  is  passed  upward,  backward,  and  inward, 
piercing  the  thin  shell  of  the  antrum  at  this  point.  The  opening  is 
made  of  convenient  size  to  admit  of  thorough  exploration.  The 
nozzle  of  an  atomizer  or  syringe,  filled  with  a  mild  antiseptic  solution, 
is  passed  into  the  antrum  and  the  cavity  is  freely  sprayeil.  A  probe 
or  the  finger  is  passed  into  the  caA'ity  and  an  ex|)loration  made  to 
detect  the  presence  of  any  dead  bone  or  bony  septi,  which,  if  found, 
must  b(>  removed,  the  cavity  of  entrance  being  enlarged  to  permit 
their  n^moNal.  After  operation  the  cavity  is  sprayed  about  every 
other  day  with  very  dilute,  warm  Dobell's  solution  or  other  mild 
sterile  solution.  (For  further  information  see  works  on  Oral  Surgery.) 
The  opening  either  heals  of  itself  or  may  be  made  to  do  so  by  the 
use  of  caustics  or  stitching  the  parts. 


552 


DISEASES  OF  THE  PERICEMENTUM 


Unless  necrosis  of  bone  occur,  cases  of  fistula  opening  upon  the 
face  or  neck  may  be  healed  by  the  ordinary  methods  carried  out 
with  extraordinary  care  to  accomplish  the  irrigation  of  the  fistula. 
The  scar  formation  is  less  than  when  extraction  is  practised  for  the 
removal  of  the  cause.  If  the  fistula  be  indolent,  the  granulations  may 
be  stimulated  by  means  of  an  injection  of  10  per  cent,  silver  nitrate 
solution.  If  the  fistula  obstinately  refuse  to  heal,  the  tooth  should  be 
extracted  and  necrosed  bone,  if  any  be  present,  surgically  removed, 
though  amputation  of  the  root  apex  may  be  tried. 


Fig.  457 


Fig.  458 


Scar  caused  by  alveolar  abscess  discharging 
on  the  face.     (Black.) 


Operation  for  the  remedy  of  scar  on  the  face 
caused  by  alveolar  abscess.     (Black.) 


Flagg*  suggested,  as  a  means  of  lessening  scar  formation,  that  a  seton 
be  passed  through  the  external  fistula  into  the  mouth,  and  that  it  be 
gradually  drawn  into  the  mouth  as  the  external  fistula  heals,  after 
which  the  tooth  is  to  be  extracted. 

In  fistulse  discharging  upon  the  face  the  formation  of  scar  tissue  may 
bind  the  tissue  of  the  cheek  tight  to  the  bone.  When  this  occurs 
beneath  the  tip  of  the  chin,  the  scar,  after  healing,  usually  resembles 
a  dimple,  and  calls  for  no  interference.  The  scar  and  binding  down 
along  the  border  of  the  inferior  maxilla,  or  beneath  the  malar  bone 
in  the  upper  maxilla,  may  produce  deformity  calling  for  remedy  (Figs. 
4r)7  and  4.'')8).  Black's  operation  is  to  be  performed  to  lessen  the 
deformitv,  for  its  complete  correction  is  not  practicable.     A  finger 


'  I^cctures 


I  )f'iital  Therapeutics. 


placed  in  the  moiitli  draws  thv  check  away  from  the  alveolar  wall,  when 
the  exact  position  of  the  cord  of  attachment  is  discovered.  A  tenotome 
knife  is  passed  into  the  tissues,  dividing  the  band  of  attachment;  a  long 
pin  is  passed  through  the  most  depressed  portion  of  the  scar,  its  centre, 
the  long  ends  of  the  pin  resting  upon  the  face;  strips  of  adhesive  plaster 
laid  upon  the  skin  under  the  head  and  point  of  the  pin  will  prevent 
the  latter  sinking  into  the  soft  tissues.  The  pin  is  retained  for  several 
days,  until  the  cut  in  the  mouth  heals.  The  principle  involved  is  the 
supplying  of  a  new  section  of  scar  tissue  which,  while  it  shi'inks, 
makes  the  total  length  of  the  cord  greater,  hence  less  binding. 

BONE  INFECTION  ASSOCIATED  WITH  DENTAL  LESIONS. 

During  the  course  of  acute  and  chronic  abscess  the  bone-marrow 
becomes  inflamed  by  the  pyogenic  organisms  and  is  broken  down 
into  pus.  The  condition  may  continue  after  extraction  for  apical 
abscess  in  the  second  stage.  It  may  also  occur  from  the  bruising  of 
the  periosteal  lining  of  the  alveolus  as  the  result  of  extraction  of  a 
hypercementosed  root,  or  from  a  bruise  induced  by  forcible  use  of 
forceps  in  the  removal  of  deeply  seated  roots. 

The  walls  of  the  alveolus  become  infected  by  pyogenic  organisms, 
among  which  the  Diplococcus  pneumoniae  figures  prominentlv.  (See 
p.  134.) 

The  leaving  of  cotton  tampons,  placed  as  vehicles  for  pain-relieving 
agents,  for  an  undue  length  of  time  also  invites  infection. 

If  during  extraction  the  alveolar  margins  be  lacerated,  and  espe- 
cially if  the  bone  be  uncovered  by  clot,  or  the  clot  fail  by  solution,  it 
also  becomes  infected  and  ulcerated,  as  shown  by  its  suppurating 
and  highly  irritable  surface;  later  the  surface  becomes  insensitive, 
indicating  superficial  necrosis,  which  may  become  progressivelv 
deeper.  Ragged  gum  margins  may  become  gangrenous,  although 
sometimes  not. 

Symptoms. — The  symptoms  are  those  of  local  inflammation  w^ithout 
necessarily  much  swelling  of  contiguous  tissues,  such  as  occurs  in 
acute  abscess.  Some  circinnscribed  swellinj;  mav  occur,  indicatinji 
an  abscess  in  association  with  it,  or  a  difl'use  swelling,  intlicating 
inflammation  of  contiguous  tissue.  The  orifice  may  appear  as  though 
normal,  but  close  examination  demonstrates  a  sinus  leading  to  ulcer- 
atetl  or  necrosed  bone.  If  due  to  an  acute  abscess  in  the  second 
stage,  the  symptoms  of  that  condition  may  continue. 


554  DISEASES  OF  THE  PERICEMENTUM 

In  the  majority  of  cases  the  pain  is  of  a  deep,  boring,  continuous 
character.  Reflex  pains  are  also  produced  about  the  face.  Much 
debiUty  is  caused  by  the  wearing  character  of  the  pain,  the  loss  of 
sleep  and  appetite,  and  probably  also  because  of  absorption  of  toxins. 
The  gum  margins  are  perhaps  sloughing ;  the  bone  may  be  exposed 
and  exquisitely  painful  to  touch,  or  it  may  be  necrotic  and  insensitive 
superficially. 

Cases  of  general  septicemic  or  pyemic  infection  from  this  source 
have  been  recorded. 

.  Treatment. — ^The  mouth  and,  in  so  far  as  possible,  the  inflamed  part 
must  be  sterilized.  Probably  mercuric  chloride  in  hydrogen  dioxide 
(1  to  1000)  will  answer  best. 

An  injection  of  a  1  or  2  per  cent,  solution  of  cocaine  into  the  healthy 
tissue  overlying  the  alveolus  will  assist  in  alleviating  the  acute  pain 
and  partly  anesthetize  the  parts.  All  sloughing  gum  should  be  cut 
away.  Exposed  bone  should  be  anesthetized  by  strong  cocaine  solu- 
tions if  painful  to  touch,  or  the  patient  should  be  anesthetized  if 
necessary.  Whether  acutely  inflamed  or  necrotic,  the  bone  should  be 
cut  away  with  large  sterile  burs  until  healthy  tissue  is  reached.  After 
washing  out  the  debris  and  further  sterilization  a  clot  is  to  be  in- 
duced by  curetting  if  necessary.  The  mouth  is  to  be  kept  sterilized 
and  the  patient  is  to  be  seen  daily  for  a  repetition  of  the  curetting. 
In  ordinary  cases  one  or  two  local  treatments  will  be  efl'ective,  but 
the  tonic,  antiseptic,  systemic  medication  recommended  under  the 
heading  of  acute  apical  abscess  is  advised. 

If  the  infection  be  of  aggravated  character,  precautions  in  the  form 
of  suitable  systemic  medication  should  be  taken  against  a  possible 
septicemia. 

If  the  patient  be  not  willing,  or  unable,  to  bear  this  operation  at  the 
first  visit  because  of  the  demoralization  produced  by  the  pain,  an 
alternative  proceeding  may  be  adopted.  A  pellet  of  cotton  wet  with 
carn[)ho-])henifjue  should  be  rolled  in  powdered  orthoform  and  intro- 
duced into  tlie  socket  after  steriUzation  with  the  mercuric  chloride 
solution,  or  a  stift'  mass  made  from  orthoform,  zinc  oxide,  and  vaseline 
may  be  packed  into  the  alveolus  as  an  antiseptic  and  anesthetic  (Jack^). 
Trichloracetic  acid  in  saturated  solution  may  be  used  to  cauterize  the 
ulcerated  surface.  The  repetition  of  this  after  five  to  eight  hours  will 
aflV)rd  marked  relief.  Later  the  radical  operation  may  be  performed 
if  gnimilation  does  not  set  in.     The  introduction  of  cotton  or  gauze 

'  International  Dental  Journal,  1905. 


NECROSIS  WITH  CHRONIC  ALVEOLODENTAL  ABSCESS      555 

dressings  into  tlie  alveoli  for  relief  of  pain  immediately  following 
extraction  is  to  be  done  only  with  extreme  care  and  for  short  periods, 
as  such  dressings  are  apt  to  be  left  in  place  by  patients,  and,  be- 
coming septic,  act  as  causes  of  sepsis  of  the  alveolar  process.  It  is 
better  to  induce  a  clot  if  the  removal  of  the  cotton  is  not  followed 
by  hemorrhage.  While  alveoli  will  fill  with  granulations  in  the 
absence  of  a  clot  filling  them,  such  a  clot  seems  to  be  the  best 
protection  against  sepsis. 

EXTENSIVE  NECROSIS  ASSOCIATED  WITH  CHRONIC 
ALVEOLODENTAL  ABSCESS. 

Every  chronic  alveolodental  abscess  carries  with  it  the  danger  of 
bone  complication.  It  has  been  shown  that  in  bone  infection  the 
organisms  are  highly  virulent.  Fortunately  in  most  cases  the  involve- 
ment is  slight  and  the  parts  care  for  themselves  when  the  cause  is 
removed.  In  more  aggravated  cases,  either  caries  or  necrosis  of  the 
bone  may  follow.  Pus  is  formed  at  the  expense  of  the  parts.  In 
caries  the  pus  escapes  by  several  fistulte,  and  examination  leads  to 
porous  dead  bone.  In  necrosis  there  is  circumvallation  of  a  portion 
or  portions  of  bone,  and  finally  one  or  more  secjiustra  are  loosened 
and  later,  in  part,  licjuefied.  The  remainder  gradually  works  out  of 
the  fistula  as  one  large  or  numerous  small  pieces.  The  patient  may 
be  much  debilitated .  In  syphilitic  cases  an  otherwise  simple  case  may 
positively  refuse  to  heal  until  the  physical  condition  is  improved  by 
antisyphilitic  and  tonic  treatment.  Surprising  recoveries  of  extensively 
necrotic  parts  occur  if  the  patient  be  brought  into  good  physical 
condition  and  the  parts  are  antiseptically  treated,  the  thorough  loosen- 
ing of  the  sequestra  being  awaited.  By  this  means  teeth  have  been 
retained  in  place  and  covered  with  new  tissue,  which  operation  woidd 
have  exposed  or  removed.  The  determination  of  the  point  at  which 
operative  interference  is  desirable  must  depend  upon  the  particular 
case  and  the  amount  of  deformity  likely  to  result  from  the  operation. 

Ilonl  and  Bukovsky  are  credited  with  the  successful  treatment  of 
bad  chronic  suppurations  by  means  of  local  applications  of  pyocyaneo- 
protein. 

Jesensky*  so  treated  a  case  of  six  months'  standing,  incurable  by 
ordinary  antiseptic  and  systemic  treatment,  and  obtained  remarknblr 
results. 

'  Dental  Cosmos,  1901. 


556  DISEASES  OF  THE  PERICEMENTUM 

S}"philitic  intoxication  may  cause  a  necrosis  of  alveolar  bone,  as  may 
mercury.  The  extent  to  which  the  teeth  or  oral  infection  act  as  active 
exciting  causes  depends  upon  the  condition  present. 


SEPTIC  APICAL  PERICEMENTITIS  COMPLICATED  BY 
PERFORATION. 

In  the  treatment  of  root  canals  the  required  mechanical  work  some- 
times results  in  (1)  the  passage  of  the  drill  through  the  apical  foramen, 
enlarging  it;  (2)  through  the  side  of  the  root,  causing  a  perforation. 

In  the  first  variety  the  complication  chiefly  concerns  the  root  filling, 
which  is  to  be  conducted  after  sterilization  upon  the  same  plan  as 
for  fining  an  unformed  foramen.     (See  p.  486.) 

If  a  lateral  perforation  be  made  near  the  root  apex,  it  may  be  filled 
after  sterilization  with  a  cone  similarly  applied,  but  made  bevelled 
at  the  end,  or  a  bit  of  aseptic  sponge  may  be  introduced  against  the 
tissue  for  a  base  and  be  covered  by  oxychloride  of  zinc.  The  packing 
of  a  fairly  stiff  mass  of  zinc  oxychloride  into  the  root  and  through  the 
perforation  into  the  fistula  has  caused  the  healing  of  several  obstinate 
cases  continually  weeping  pus  or  serum.  The  same  treatment  used 
with  greater  care  is  useful  in  chronic  abscesses  without  fistula.  It  is 
well  to  only  fill  the  apical  portions  of  canals  in  either  case,  so  that  any 
removal  for  another  trial  may  not  be  too  difficult;  the  later  filling  of 
the  coronal  portion  of  the  canal  is  very  simple.  The  use  of  a  stift' 
paste  of  zinc  oxide  and  eugenol  or  even  oxyphosphate  of  copper  in 
the  same  manner  is  useful.  If  possible,  it  is  well  to  irrigate  the  fistula 
with  water  to  remove  any  excess,  though  if  left  it  usually  works  out 
of  the  fistula,  which  later  heals  or  not,  as  the  case  may  be.  If  septic 
conditions  persist,  the  root  end  must  be  amputated,  or  the  tooth 
extracted,  prepared,  and  replanted.  If  made  in  the  middle  third  of 
the  root,  the  canal  must  be  sought  fox*  and  treated  as  usual  beyond 
the  perforation,  which  is  then  separately  treated  with  a  gutta-percha 
cone,  or  a  plaque  of  gutta-percha  may  be  laid  over  the  perforation 
and  antiseptic  cements  or  copper  amalgam  used  to  secure  it  in 
position.  Extraction  and  replantation  may  be  resorted  to,  but 
amputation  does  not  serve  so  well,  as  the  root  leverage  is  lost  and  the 
tooth  may  loosen.  In  a  favorable  case,  after  canal  exploration,  a 
tapering  probe  may  be  passed  into  the  canal  and  copper  amalgam 
gently  tamped  a})out  it  and  against  the  perforation;  the  probe  is  then 


CHRONIC  SEPTIC  APICAL  PERICEMENTITIS 


557 


withdrawn,  leaving  a  central  canal,  which  is  later  treated.  Girdwood 
has  reported  good  results  from  the  nse  of  copper  amalgam  which,  in 
this  connection,  the  writer  can  confirm.  In  a  few  cases  the  fistula 
has  been  packed  open  and  the  perforation  filled  with  amalgam. 
The  cases  are  mostly  successful,  but  in  one  case  healing  did  not  occur 
until  treatment  after  filling  was  suspended  for  several  months. 

Chronic  Septic  Pericementitis  in  the  Temporary  Teeth.— Any  o^ 
the  chronic  se})tic  conditions  described  may  occur  upon  the  temporary 
teeth.  The  presence  of  resorption  and  of  the  permanent  crown  usually 
confines  the  inflammation  to  a  point  lower  in  the  alveolar  process 
than  in  the  case  of  permanent  teeth.  The  loose  character  of  the 
structure  causes  the  ulceration  to  occupy  a  larger  area,  and  the  parts 
in  chronic  inflammation  look  more  angry,  but  are  fairly  well  tolerated. 
The  treatment  is  practically   the  same  for  the  curable  cases;  the 


Fig.   459 


Fig.  460 


Skiagrapli  of    crowned    furve<l    root,    with 

perforation  and  protruding  root    filling    near  Showing  the  relations  of  an  abscess  upon  a 

apical  foramen,  with  septic  conditions,  would  temi)orary  tooth,  with  the   crown  of  a   devel- 

require  root  amputation.      (Price.')  oping  permanent  tooth  un<lerl.ving  it. 

others  should  be  extracted.  The  root  canals  when  treated  should 
be  filled  with  absorbable  materials  such  as  paraffin  or  wax  combined 
with  aristol.  Buckley  recommends,  as  a  canal  filling  in  these  cases, 
the  u.se  of  a  stiff  mixture  of  calcium  phosphate  and  formo-cresol 
(formalin,  1  part;  cresol,  1  or  2  parts),  to  be  packed  into  the  pulp 
chamber  and  zinc  })hosphate  (juicklv  flowed  over  it;  the  cavitv  to  be 
filled  later. 

Johnson"  suggests  that  a  eucalyptol  solution  of  gutta-percha  (see 
p.  4S7)  be  ])umped  into  the  canals  and  pressure  exerted  with  tempo- 
rary stopping  until  the  .solution  appears  at  tlie  fistula.  The  temj)or;irv 
stopping  diat  does  not  interfen*  with  filling  integrity  should  be  left. 

Chronic  Septic  Apical  Pericementitis  (Non-purulent).— Con- 
tinued infiannnation  of  a  low  grade  (interstitial   gingivitis),  or  what 


1  Items  of  Interest,   1901. 


Dental  Cosmos,  1S99. 


558 


DISEASES  OF  THE  PERICEMENTUM 


may  in  reality  be  continued  atonic  hyperemia,  may  exist  in  the  apical 
pericementum  for  long  periods  without  pus  formation. 


Fig.  461 


a 


Fig.  462 


Dentine  from  the  root  of  an  abscessed 
tooth,  showing  the  penetration  of  cocci  to  a 
depth  of  about  j^q  mm.  (..i^r)  ^^•)'>  the  side 
a-b  bordered  upon  the  canal.  X  1000. 
(Miller.) 


1,'i 


Cause  and  Pathology.  —  The 
cause  consists  of  unremoved  gan- 
grenous pulp  tissue,  septic  serous 
collections  in  canal  apices  or  about 
imperfect  root  fillings,  or  septic 
material  in  the  root  tubuli,  all 
much  the  same  in  character.  A 
very  common  cause  is  an  other- 
wise good  root  filling  which  has 
failed  to  fill  the  apical  portion 
of  a  curved  fine  or  even  well- 
opened  root.  While  in  skilful 
hands  gutta-percha  points  and 
oxychloride  of  zinc  usually  reach 
their  apical  destination,  the  editor 

has    met   unfilled   apical    canals  after  good  operators  as  the  most 

common  of  operative  errors. 


Sector  of  a    cross-section    from  a    diseased 
root:   a,  cementum;   b,  stratum   granulosum; 

c,  very  narrow  and    finely  branched  tubules; 

d,  penetration  of    bacteria  into    tubules.      X 
150.     (Miller.) 


CHRONIC  SEPTIC  APICAL  PERICEMENTITIS  .J59 

An  imperfectly  filled  perforation  may  cause  a  similar  condition, 
which,  however,  the  a;-rays  should  determine. 

Albuminous  fluid  may  enter  the  canal  via  the  apical  foramen,  and, 
becoming  infected,  putrefaction  ensues.  The  source  of  infection  may 
possibly  be  via  the  blood,  but  leaking  crown  and  root  fillings  more  prob- 
ably permit  bacteria  to  enter  from  the  mouth.  The  more  or  less  constant 
result  of  filling  roots  with  cotton  permeated  with  evanescent  materials 
only  is  evidence  of  this.  The  cotton  absorbs  fluid  either  from  about 
leaky  fillings,  too  often  placed  in  contact  with  it,  or  else  from  the  apical 
tissues;  infection  readily  occurs  and  a  highly  odorous  cotton  is  removed 
because  of  the  apical  irritation.  When  the  cotton  is  well  placed  and 
confined  under  tight-sealing  materials  to  the  apical  half  of  the  root 
canal,  this  result  is  long  delayed  in  many  cases.  Portions  of  gangren- 
ous pulps  remaining  in  canals  may  likewise  become  infected.  Extra 
and  untreated  canals  are  frequently  causes. 

Miller^  has  shown  that  root  tubules  are  infected  only  for  a  short 
distance  at  their  canal  ends,  so  that  infection  from  the  pericementum 
via  the  cementum  and  dentinal  tubules  is  highly  improbable  (Fig. 
461).  The  putrefaction  produces  gases,  and  these  exuding  slowly  pro- 
duce the  irritation.  If  pyogenic  organisms  be  present,  apical  abscess 
may  at  any  time  supervene. 

Symptoms. — Subacute  inflammation  of  apical  tissue  being  present, 
the  symptoms  of  this  condition  are  tenderness  upon  decided  pressure 
or  upon  percussion;  the  response  may  only  be  elicited  by  pressure 
or  percussion  in  one  direction.  The  tooth  gives  a  dull  note  upon 
percussion,  and  is  usually  looser  than  its  neighbors.  The  red  line  of 
the  gum  extends  farther  toward  the  gum  margin  than  normal — cjuite 
to  it  in  some  cases. 

Some  slight  looseness  may  be  noted  and  the  patient  is  apt  to  avoid 
the  tooth  in  mastication.  In  some  cases  acute  reflex  pains  in  other 
teeth  may  precede  an  outl)reak  of  purulent  })ericementitis,  a  frc(|uent 
secjuel  to  this  condition.  There  are  also  evidences  of  previous  devital- 
ization of  the  pulp  in  opacity,  lack  of  response  to  tests  for  vitality,  etc. 
At  times  a  history  of  previous  canal  treatment  may  be  obtained  or  the 
evidences  of  an  attempt  at  canal  filling  may  be  seen  upon  opening  the 
tooth. 

Diagnosis. — The  condition  rec|uires  careful  dilVerentiation  from 
(1)  non-septic  apical  jx-ricemenfitis  (hie  to  traumatism  or  maloc- 
clusion or  to  a  perforation  imperfectly  filletl;  (2)  pericemental  abscess 

I  Deutal  Cosmos,  1899. 


560  DISEASES  OF  THE  PERICEMENTUM 

in  the  early  stage ;  (3)  abscess  of  the  pulp  in  the  later  stages.  In  nearly- 
all  these  cases  the  pulp  may  be  vital.  Being  itself  only  subsequent  to 
death  of  the  pulp,  tests  for  vitality  are  made.  (See  p.  496.)  If  pulp 
death  be  indicated  by  the  tests,  the  pulp  canal  is  explored,  and,  if  found, 
treated  and  filled;  a  septic  condition  about  or  beyond  the  same  is 
looked  for. 

There  is  great  disadvantage  in  a  large  apical  opening,  particularly 
in  the  dressing  and  root-filling  operation. 

Treatment. — The  condition  being  analogous  to  that  of  moist  gan- 
grene, the  treatment  is  the  same.  Before  it  can  be  appHed  the  root 
canals  should  be  opened,  and  to  accomphsh  this  all  root  fillings 
involved  require  removal.  If  an  extra  canal  be  found  after  apparently 
conscientious  w^ork  has  been  done,  this  should  receive  attention  before 
removing  root  fillings. 

The  bulk  of  gutta-percha  root  filUngs  are  best  drilled  out  with 
Gates-Ghdden  drills  revolved  in  the  engine  hand-piece.  Where  they 
extend  beyond  the  reach  of  the  finest  drill  the  finest  Downie  broach 
may  be  used,  or  the  broach  may  be  used  to  drive  eucalyptol  into  the 
gutta-peicha  to  dissolve  it.  The  Downie  broach  is  far  safer  than  the 
Gates-Glidden  drill. 

All  cement  fillings  are  removed  by  a  drill  so  far  as  can  be  safely 
done,  dryness  being  a  great  aid  in  locating  the  cement  in  the  canal. 
When  the  danger  of  perforation  arises,  a  stiff  Swiss  broach  or  a  fine 
Downie  broach  may  be  rubbed  down  to  a  drill  edge  and  used  as  a 
tamp  drill.  Sulphuric  acid  in  50  per  cent,  solution  or  aqua  ammonia 
aid  by  dissolving  the  cement. 

The  object  sought  for  is  an  unfilled  canal  lumen,  which,  when  found, 
is  readily  recognized  by  the  ease  of  penetration  with  the  broach  and 
the  absence  of  sensation  until  the  apical  tissue  is  reached. 

There  can  be  no  assurance  of  safety  until  the  apical  tissue  can  be 
explored,  but  perforaHon  must  be  avoided.  The  fine  Downie  broach  is 
useful  in  difficult  cases,  and,  if  necessary,  a  No.  1  Beutelrock  drill  may 
be  used.  When  the  apical  foramen  is  open,  or  further  work  is  im- 
possible without  the  danger  of  perforation,  the  canal  treatment  is 
confhicted  upon  the  lines  laid  down  for  gangrenous  pulp.  (See  p.  503.) 
A  difficult  class  of  cases  sometimes  presents  in  which  the  disease 
supervenes  and  where  work  which  may  be  regarded  as  desperate 
has  been  done,  or  where  pins  have  been  inserted  and  are  almost 
impossible  of  removal,  as,  for  example,  where  a  IvOgan  crown  has  been 
cemented  to  place.     In  such  cases  the  idea  of  Watkins  in  applying 


CHRONIC  SEPTIC  APICAL  PERICEMEXTITIS  561 

blue  light  directly  bv  means  of  a  funnel  may  V)e  of  great  value  in 
reducing  inflammation,  and  mild  applications  of  the  a--rays  may  be 
useful,  but  sometimes  the  work  must  be  carefully  dismantled  to  permit 
re-treatment.    An  r-ray  should  always  be  first  made  as  a  guide. 

If  the  pericementitis  have  been  of  long  standing,  the  thickening  of 
the  membrane  will  have  caused  protrusion  of  the  tooth.  The  tooth 
should  be  ground  off  at  its  point  of  occlusion  until  it  occludes  with 
somewhat  less  force  than  its  neighbors,  the  therapeutic  principle  in 
these  cases  being  that  of  removing  the  source  of  irritation  and  procuring 
surgical  rest.  Indications  of  favorable  results  are  found  in  the  red 
gum  hne  assuming  its  normal  position,  tenderness  disappearing,  and 
increased  tightness  of  the  tooth. 

This  aHection  is  extremely  common  about  the  roots  of  pulp  less 
teeth,  and  always  signifies  more  or  less  enforced  disuse  of  the  teeth, 
and,  if  uncorrected,  their  ultimate  loss. 

This  condition  is  sometimes  associated  with  a  chronic  swelling, 
probably  cystic  in  character,  upon  the  gum,  simulating  an  acute  abscess 
in  local  appearance,  but  the  contiguous  tissues  are  not  involved.  The 
swelling  may  have  the  size  of  a  hazelnut.  Upon  treatment,  acute 
apical  abscess  is  apt  to  be  lighted  up;  therefore  the  sterilization  by 
cataphoresis,  or  by  25  percent,  pyrozone,  should  be  prolonged  and  the 
swelling  should  be  promptly  opened  by  a  deep  incision,  thus  establish- 
ing an  artificial  fistula.  In  one  case  of  one  year's  standing,  associated 
with  a  lower  molar  tooth  which  had  a  leaky  gutta-percha  crown  and 
partial  canal  filling,  extraction  was  advised  for  reasons  other  than 
canal  treatment.  The  cyst  then  promptly  developed  as  an  acute 
abscess,  which  shifted  its  position  toward  the  cheek  and  there  dis- 
charged without  production  of  scar. 

Septic  Pericementitis  at  Bifurcations  of  Multi-rooted  Teeth. — 
Teeth  weakened  bv  caries  may  fraciure  after  fillino:  in  such  a  manner 
that  the  line  of  fracture  ex-poses  the  pericementum  at  the  bifurcation. 
The  crack  admits  septic  saliva,  and  a  filling  or  fillings  usually  sink, 
gingivally  wedging  apart  the  two  sections  and  admitting  more  or  less 
food  matter.  If  the  canals  of  the  sections  have  been  previously  treated 
ant!  filled,  it  is  usual  to  find  a  more  or  less  general  pericementitis 
due  lo  the  wedging  and  septic  irritation.  It  subsides  upon  sterilizing 
by  means  of  adouch,  while  gentle  broaching  removes  the  accumulated 
debris.  Tricresol  and  formalin,  diluted  with  phenol  camphor  to  a 
5  or  10  per  cent,  formalin  strength,  is  to  be  placed  in  the  pulp  cavity 
and  covered  with  sandarached  cotton,  and  a  ligature  of  silk  or  wire 
36 


562  DISEASES  OF  THE  PERICEMENTUM 

is  to  be  tied  about  the  tooth  to  draw  the  parts  together.  A  hollow 
metal  crown  is  to  be  constructed,  and  before  placement  a  little 
ox}'phosphate  of  copper  or  oxychloride  of  zinc  cement  is  to  be  worked 
into  the  joint  which  is  temporarily  sprung  open. 

If  the  canals  be  septic,  an  apical  abscess  may  complicate  the  condi- 
tion and  require  treatment  while  the  fracture  is  being  handled.  In 
some  cases  a  metal  staple  may  be  placed  in  the  canals  of  the  two 
sections  and  so  arranged  as  to  spring  the  parts  together  when  forced 
to  place.  The  joint  should  have  one  of  the  cements  worked  into  it 
before  this  staple  is  cemented  to  place.  About  the  staple  quick- 
setting  amalgam  should  be  packed,  a  copper  band  having  been  pre- 
viously adjusted  to  act  as  a  matrix.  Later,  this  band  is  to  be  removed 
and  a  porcelain-faced  gold  crown  or  a  porcelain  crown  baked  on  a 
heavy  wide  platinum  band  and  cap  arranged  to  sustain  it. 

The  staple  may  be  utilized  as  a  portion  of  a  crown  base  of  the 
Richmond  or  other  variety,  the  bifurcation  and  crown  cementing  being 
deferred  until  the  final  operation.  Irritation  may  arise  in  some  of 
these  cases,  which,  however,  need  not  prevent  the  trial  of  the  method 
as  a  last  resort. 


CHAPTER  XXI. 
NON-SEPTIC  PERICEMENTITIS. 

Various  grades  of  pericemental  irritation,  ranging  from  a  mild 
arterial  hyperemia  to  actual  inflammation,  may  be  produced  by  non- 
septic  causes. 

The  most  satisfactory  evidence  that  inflammation  may  be  so  caused 
is  furnished  by  Talbot's  experiments  with  the  mercurialization  of  dogs. 
Beginning  with  healthy  pericementi,  these  were,  after  mercurialization 
of  the  animal,  found  to  contain  the  round-celled  infiltration  character- 
istic of  inflammation,  and  no  bacteria  could  be  found.  Further  evi- 
dence is  given  by  the  usual  experimental  study  of  inflammation  with 
the  mesentery  of  the  frog.  Simple  irritation,  even  with  antiseptic 
substances,  produces  the  phenomena.  Any  of  the  causes  which  may 
produce  inflammation  may,  if  acting  in  more  mild  degree,  produce 
arterial  hyperemia.  If  the  action  of  the  cause  be  violent  and  then 
discontinued,  as  in  the  case  of  a  blow,  the  inflammation  resulting  is 
acute,  but  may  pass  into  a  chronic  form;  but  if  the  cause  continue  to 
act  it  produces  a  chronic  inflammation. 

For  purposes  of  description,  non-septic  pericementitis  may  be 
divided,  according  to  its  character,  into  traumatic  and  symptomatic, 
and,  according  to  its  location,  into  apical  and  general. 

TRAUMATIC  PERICEMENTITIS. 

By  traumatic  pericementitis  is  meant  a  profound  irritation  of  the 
pericementum,  the  result  of  mechanical  violence  applied  externally  to 
the  tooth,  or  of  instrumentation  or  chemical  irritation  of  the  peri- 
cementum through  the  root  canal. 

Causes. — Violence  Externally  Applied. — Excessive  force  deliv- 
ered directly  upon  the  teeth,  as  in  case  of  blows,  falls,  overmalleting 
in  building  fillings,  the  biting  of  nuts,  thread,  or  other  hard  objects, 
or  force  indirectly  delivered,  as  in  case  of  blows  received  under  the 
chin,  bringing  the  teeth  forcibly  together,  may  all  cause  acute  peri- 
cementitis. 


564  DISEASES  OF  THE  PERICEMENTUM 

An  excessive  amount  of  filling  on  the  occlusal  surface  of  a  tooth, 
a  maloccluding  crown  or  overfull  fillings  upon  the  proximal  aspect, 
maintaining  a  wedged  condition,  cause  overocclusion  upon  the  tooth 
and  an  irritation  of  its  pericementum. 

The  overstraining  of  the  pericementum  of  a  tooth  as  the  result  of 
overuse,  as  in  cases  where  only  a  few  teeth  remain  for  mastication,  or 
where  pyorrhea  or  calculus  has  caused  resorption  of  the  alveolar 
process  and  looseness  of  the  teeth,  or  where  artificial  dentures  are 
clasped  to  remaining  teeth,  or  where  bridges  are  supported  upon 
insufficient  piers,  are  frequent  causes  of  non-septic  pericementitis  of  a 
degenerative  character.  The  presence  of  a  rough  flaring  or  a  too 
deeply  placed  crown  band  beneath  the  gum  margins,  portions  of 
cement  used  in  cementation  of  crowns,  or  excess  of  filling  material 
beneath  the  gum,  are  all  causes  of  marginal  gingivitis,  with  which 
pericementitis  may  be  associated.  With  these  marginal  cases  septic 
causes  usually  have  to  be  considered  as  complications. 

Too  violent  wedging  is  always  followed  by  more  or  less  pericementitis 
of  the  wedged  teeth  and  their  neighbors,  more  marked  when  elastic- 
rubber  wedges  are  used. 

In  correcting  irregularities  of  the  teeth,  if  they  be  moved  too  rapidly, 
are  not  firmly  directed  dui-ing  the  operation,  or,  subsequently,  not 
firmly  maintained  in  position,  pericementitis  of  a  high  grade  is  fre- 
quently excited. 

Violence  Internally  Applied. — If  a  wholly  or  partially  vital 
pulp  be  torn  from  its  apical  connections,  as  in  the  use  of  pressure 
anesthesia,  an  apical  traumatic  pericementitis  may  be  set  up.  This 
is  usually  transient.  Secondary  hemorrhage  may  occur  and  produce 
pericementitis. 

Excessive  laceration  of  the  apical  tissue  by  means  of  barbed  instru- 
ments, the  inclusion  of  air  or  medicament  under  a  root  dressing  or 
fining,  the  same  exercising  pressure  upon  the  apical  tissues;  the 
mechanical  irritation  of  a  projecting  root  filling,  pivot  wire,  broach,  or 
drill,  are  all  sufficient  causes. 

The  undue  enlargement  of  the  apex  of  the  root  canal  or  the  passage 
of  a  reamer  through  the  lateral  aspect  of  a  root  may  excite  inflam- 
niatioi),  and  the  pei-fcct  filling  of  the  opening  may  be  exceedingly 
difficult,  so  that  if  the  tissues  are  not  infected  at  the  time,  sepsis  may 
later  follow.  ^ 

Chemical  Irritation. — ^^rhe  application  of  arsenic  to  a  perforation 
may  excite  inflammation  and   necrosis.     (See  p.  473.)     The  use  of 


TRAUMATIC  PERICEMEXTITIS  565 

arsenic  as  a  pulp  devitalizer  may  cause  a  hyperemia  of  the  apical 
tissue,  following  the  hyperemia  of  the  pulp,  and  causing  slight  tooth 
extrusion,  which  is  aggravated  by  the  malocclusion. 

The  undue  use  of  escharotics,  such  as  carbolic  acid,  sodium  dioxide, 
zinc  chloride,  sulphuric  acid,  or  mercuric  chloride,  in  a  pulp  canal 
may  excite  an  undesirable  irritation.  The  limited  irritation  following 
their  limited  use  is  often  more  dian  oli'set  by  the  advantages  of  the 
asepsis  produced. 

Prophylaxis. — Many  of  these  causes  are  avoidable,  and  operators 
mindful  of  possible  irritations  should  avoid  the  mechanical  irritation 
of  apical  tissues,  neutralize  powerful  acids  or  alkalies,  use  escharotics 
with  caution,  wedge  teeth  gradually,  ami  after  wedging  either  pack 
gutta-percha  between  the  teeth  to  permit  them  to  rest  for  a  few  days 
or  fix  them  immovably  w^th  wooden  wedges  or  steel  separators  during 
malleting. 

During  orthodontia  teeth  shoidd  be  moved  steadily,  and  after  align- 
ment is  secured  they  should  be  firmly  maintained  in  position  until 
deposition  of  bone  occurs. 

Patients  should  be  warned  against  the  evil  effects  of  thread  biting 
and  biting  hard  substances. 

Pathology  and  Morbid  Anatomy. — Chemical  substances  applied  in 
excess  cause  a  destruction  of  tissue  dependent  upon  the  quantity  used. 
Inflammation  tending  to  the  resorption  of  the  dead  tissue  occurs.  The 
pericementitis  presumably  persists  in  some  degree  until  the  foreign 
(dead)  material  is  removed  by  natural  processes. 

In  the  case  of  protruding  foreign  bodies,  such  as  root  fillings,  broaches, 
etc.,  there  is  a  tendency  of  the  inflammation  to  become  subacute  or 
chronic.  The  foreign  body  may  to  an  extent  become  encysted, 
particularly  in  the  case  of  a  gutta-percha  root  filling.  In  other  cases 
the  continued  vascular  disturbance,  if  of  mild  degree,  produces  hyper- 
cementosis;  in  more  severe  cases  resorption  of  the  root  occurs. 

In  the  case  of  arsenic  it  is  to  be  remembered  that  the  arsenic  does 
not  pass  the  point  of  constriction,  and  no  fear  should  be  felt.  (See 
p.  472.) 

Cases  due  to  perforation  of  the  root  and  wounding  of  the  peri- 
cementum, after  the  acute  symptoms  have  passed,  commonly  assume 
an  irritative  and  chronic  type,  the  soft  tissues  included  in  the  perfora- 
tion being  in  a  state  of  chronic  inflammation.  Many  of  these  cases 
become  infected  owing  to  the  difficulty  of  completely  sterilizing  the 
apical  portion  of  the  canal  which  lies  beyond  them. 


566  DISEASES  OF  THE  PERICEMENTUM 

The  pericementitis  produced  by  pressure  of  included  air,  liquid,  or 
plastic  root  filling  upon  the  apical  tissue  is  often  severe.  Upon  removal 
of  the  root  dressing  or  filhng  the  engorgement  is  relieved  by  the  gushing 
of  blood  through  the  root  canal.  The  inflammation  may,  however, 
continue  unless  sedatives  be  applied  to  the  apical  tissue  via  the 
canal. 

In  cases  due  to  traumatism,  such  as  violent  wedging,  rapid  move- 
ment in  regulating,  overmalleting,  blows,  biting  of  thread,  ice,  nuts, 
etc.,  the  condition  is  surgically  one  of  bruise. 

The  phenomena  of  active  inflammation  make  their  appearance  to  an 
extent  governed  by  the  degree  of  violence — exudation,  swelling,  red- 
ness, and  pain;  fibrinous  and  corpuscular  exudations  occur,  and  later  a 
reorganization  of  tissue  occurs,  in  some  cases  a  degeneration,  depend- 
ing upon  the  completeness  with  which  the  indicated  therapeusis  is 
applied  and  upon  the  vitality  of  the  patient. 

Traumatic  pericementitis  in  high  degree  in  the  young  may  be 
recovered  from;  but  in  the  middle-aged  and  aged  it  may  give  rise  to  a 
series  of  degenerative  changes  which  only  end  with  the  loss  of  the  tooth. 

In  cases  due  to  looseness  of  the  teeth,  of  course,  septic  primary 
causes  have  to  be  considered,  but  the  pericementitis  may  be  quite  as 
much  mechanically  as  septically  produced. 

In  all  cases  the  extrusion  caused  by  the  inflammation  adds  another 
exciting  cause  of  apical  pericementitis — i.  e.,  malocclusion,  which 
aggravates  the  condition. 

Symptoms  and  Diagnosis  .^ — The  amount  of  pericemental  inflamma- 
tion present  is  evidenced  by  the  soreness  and  extrusion  of  the  tooth 
and  the  degree  of  redness  in  the  overlying  gum  tissue. 

A  history  of  violence  may  be  obtained  when  it  has  occurred.  Mal- 
occlusion may  be  detected  by  occlusion  marks  upon  fillings  or  by 
means  of  carbon  paper.  The  untoward  results  of  canal  operations 
may  be  inferred  from  a  personal  knowledge  of  the  case  or,  perhaps, 
from  the  history.  It  is  at  times  difficult  to  exclude  septic,  non-purulent, 
apical  pericementitis  as  a  cause,  particularly  if  the  case  come  from  the 
hands  of  another  practitioner.  In  doubtful  cases  the  treatment  for 
inferred  traumatisms  may  be  employed,  and  if  followed  by  good 
results  a  fost  hoc  diagnosis  of  traumatic  pericementitis  may  be  made. 
The  x-rays  afl'ord  a  means  of  determining  extruding  root  fillings, 
broaches,  etc.  (Figs.  481  and  459). 

Treatment. — Foreign  bodies  protruding  fi'oin  the  root  apex  must  l)e 
removed  if  persistent  symptoms  demand  it.     'J^his  may  require  an 


TRAUMATIC  PERICEMENTITIS  507 

artificial  opening  for  its  performance,  or  root  amputation.  Perfora- 
tions should  be  carefully  treated. 

If  evidence  of  pericementitis  persist,  the  end  of  the  root  including 
the  perforation  should  be  amputated  or  the  tooth  may  be  extracted,  the 
perforation  and  canal  filled  with  gold  or  gutta-percha,  and  the  tooth 
replanted  under  antiseptic  precautions. 

In  all  cases  due  to  violence  the  treatment  is  that  adapted  to  injury; 
first,  surgical  rest  of  the  pericementum.  This  may  be  accomplished 
in  two  ways:  either  by  preventing  the  tooth  striking  its  antagonists 
or  holding  it  so  rigidly  that  it  cannot  move  if  it  does  meet  them.  As 
a  prehminary  measure  the  tooth  is  gently  but  firmly  lashed  to  its 
neighbors  by  means  of  ligatures  so  that  it  is  rigidly  held.  A  swaged 
cap  is  either  fitted  to  a  neighboring  tooth,  or  the  antagonizing  teeth  are 
ground  away  until  they  fail  to  strike  the  injured  tooth;  the  first  method 
is  to  be  preferred. 

In  cases  involving  several  teeth,  such  as  all  of  the  incisors,  two 
metallic  plates  are  quickly  swaged  to  cover  posterior  teeth  and  raise 
the  bite,  and  they  are  cemented  in  position  to  relieve  the  irritated 
•teeth  from  occlusion. 

When  the  apical  tissues  have  been  irritated  by  way  of  the  canal, 
sedatives,  such  as  strong  tincture  of  aconite  or  menthol  in  chloroform 
or  menthol-phenoP  (menthol,  3  parts;  carbolic  acid,  1  part;  melted 
together),  should  be  applied  on  cotton  to  the  apical  tissue  by  way  of 
the  root  canal.  The  addition  of  iV  grain  of  cocaine  hydrochlorate  to 
one  of  the  above  sedatives  will  notably  increase  its  action.  It  may 
either  be  rubbed  into  the  fluid  or,  preferably,  be  taken  up  upon  the  point 
of  the  cotton  twist  introchiced  into  the  canal.  All  cases  of  traumatic 
pericementitis  require  the  persistent  use  of  counterirritants  applied 
every  other  day  to  the  overlying  gum. 

Systemic  derivation  is  also  useful  in  the  acute  cases.  In  even  mild 
cases  not  due  to  violence  the  guarding  of  the  extrudeil  tooth  against 
malocclusion  is  of  advantage. 

If  the  cause  be  some  mechanical  irritant  at  tlu>  gum  margin,  this 
should  be  removed  and  the  case  treated  as  above  described .  Ricogni/- 
ing  the  ]K)ssil)le  influence  of  septic  causes,  oral  antiseptics  aiv  to  be 
used . 

*  Dr.  Morgan  TTowe. 


568  DISEASES  OF  THE  PERICEMENTUM 


SYMPTOMATIC  NON-SEPTIC  PERICEMENTITIS. 

By  symptomatic  non-septic  pericementitis  is  meant  an  aseptic  peri- 
cementitis occurring  as  the  result  of  systemic  conditions,  or  of  the 
action  of  drugs  taken  internally. 

If  mercury  be  administered  to  patients  in  large  doses  for  long 
periods,  or  in  one  or  more  massive  doses,  or  if  the  patient  have  an 
idiosyncrasy  to  the  action  of  this  agent,  an  irritation  of  the  salivary 
glands  is  excited,  followed  by  looseness  and  soreness  of  the  teeth  and 
swelling  of  the  gums;  that  is,  a  general  pericementitis  and  maxillary 
periostitis  arise.  The  patient  has  a  metallic  coppery  taste,  coated  tongue, 
and  fetid  breath;  the  gums  are  puffy  and  bleed  easily.  In  advanced 
cases  the  tongue  and  cheeks  are  swollen.  Potassium  iodide  administered 
in  this  condition  relieves  the  maxillary  periostitis  and  pericementitis; 
but  the  same  drug  administered  in  health,  or  for  conditions  other  than 
mercurial  poisoning,  also  causes  irritation  of  the  pericementum. 
Pilocarpine  has  a  similar  effect,  though  in  much  less  degree.  All  of 
these  drugs  are  partially  eliminated  by  the  glandular  appendages  of 
the  mouth,  and  during  elimination  apparently  act  as  local  irritants. 
Lead  poisoning  may  have  a  similar  action. 

Patients  who  have  a  gouty  heredity,  or  who  are  the  subjects  of 
active  gout,  frequently  exhibit  a  tenderness  of  the  entire  pericementum 
of  one  or  more  or  sometimes  all  of  the  teeth.  This  pericemental  dis- 
turbance may  be  the  precursor  of  an  acute  outbreak  of  gout  in  the 
metatarsophalangeal  joint. 

Scurvy — a  very  rare  systemic  disease — is  attended  by  rapid  de- 
generation of  the  pericementum  of  the  teeth  and  of  the  alveolar 
tissues. 

Syphilis  is  also  attended  by  pericemental  irritation.  This,  of  course, 
is  of  septic  origin. 

Talbot's  experiments  on  dogs  show  conclusively  that  a  true  peri- 
cementitis may  be  induced  owing  to  the  chemotactic  properties  of  the 
mercury  alone.     (See  Interstitial  Gingivitis.) 

In  auto-intoxication  by  intestinal  toxins  or  by  leucomaines  in  diseases 
involving  general  malnutrition,  the  irritants  are  probably  in  part 
eliminated  by  the  gums,  which  are  in  turn  irritated.  (See  Gouty  Peri- 
cementitis.) 

It  has  been  shown  by  Ivoup  that  mercurial  stomatitis  may  be  cured 
by  mercury  used  as  an  oral  antiseptic;  therefore,  the  logical  conclusion 


HYPERCEMENTOSIS  569 

is  that  oral  organisms  play  a  part  in  the  production  of  the  local 
effects  of  mercury;  probably  the  mercury  produces  a  local  predis- 
position. 

Treatment. — The  drug  should  be  discontinued,  the  disease,  if  pres- 
ent, should  be  antagonized,  and  the  local  complications,  if  any,  should 
be  appropriately  treated,  antisepsis  being  always  advisable.  If  the 
pericementitis,  gingivitis,  and  stomatitis  be  mercurial,  the  drug  should 
be  stopped  and  an  antisialagogue  used,  such  as  atropine  sulphate, 
T"uir  gr.  each  four  to  six  hours,  until  relieved. 

Potassium  chlorate  as  a  mouth  wash,  or  internally,  is  useful  if  the 
stomach  is  not  irritable. 

I^. — Potasii  chlorat gr.  xlviij 

Tr.  myrrh fS^s 

Elixir  calisayae q.  s.  ad    fgiij — M. 

Sig. — Teaspoonful  every  five  hours,  or  use  as  a  mouth  wash.      (Hare.) 

Results  of  Chronic  Non-septic  Pericementitis. — If  at  any  point  of  the 
irritated  pericementum  a  constructive  grade  of  irritation  be  maintained, 
the  cemental  tissue  becomes  hj^ertrophied  (Fig.  463).  If  a  more 
severe  grade  of  irritation- — i.  e.,  low-grade  inflammation  (interstitial 
gingivitis) — be  present  for  a  long  time,  the  cementum  and  even  the 
dentine  of  the  root  may  be  resorbed.  Both  of  these  results  may  go  on 
concurrently  at  different  points,  or  resorption  may  be  followed  by 
deposition  of  cementum  if  the  conditions  change. 

Chronic  overuse  or  disuse  of  teeth  result  in  degenerations  of  the 
pericementum  through  a  process  of  interstitial  gingivitis,  including 
pericementitis. 


HYPERCEMENTOSIS  (DENTAL  EXOSTOSIS,  EXCEMENTOSIS, 
HYPERPLASIA  OF  THE  CEMENTUM). 

Definition. — By  hype rce men tosis  is  meant  a  secondary  deposit,  or 
an  increase  of  volume  of  the  cementum  of  a  tooth  beyond  the  normal 
limit.     It  may  be  circumscribed  or  difi'use. 

Causes. — A  mild  or  constructive  degree  of  irritation  is  the  proximate 
cause,  which  may  be  excited  by  numerous  primary  causes,  such  as  a 
projecting  root  filling,  a  projecting  edge  of  crown  filling,  deposits  of 
salivary  calculus,  the  overlapping  of  a  cavity  margin  by  the  gum,  mal- 
occlusion, non-occlusion,  the  biting  of  hard  objects,  such  as  nuts  or 
thread,  the  overuse  of  certain  teeth,  the  habitual  tapping  together  of 
teeth,  the  habitual  chewing  of  toothpicks,  the  graihial  pressure  of 


570 


DISEASES  OF  THE  PERICEMENTUM 


gas  from  dead  pulps.  The  pressure  of  a  tooth  root  against  another 
root  during  eruption  is  a  sufficient  cause,  (See  Fig.  190.)  The 
overcrowding  of  teeth  in  an  arch  has  also  caused  this  condition, 
as  has  also  the  impaction  of  a  tooth  (Fig.  220).  Chronic  alveolar 
abscess  or  pyorrhea  alveolaris  may  cause  it  by  inducing  about 
itself  at  a  distance  an  area  of  hyperemia.  Interstitial  gingivitis 
is  also  a  cause.  It  also  seems  at  times  to  be  induced  after  pulp 
devitalization  from  any  cause.     H^'percementosis  •  is  a  possibility  in 

Fig,  463 


any  case  of  chronic  pericemental  irritation;  it  represents  a  degree 
of  irritation  rather  than  any  one  specific  cause.  It  has  b^en  discussed 
by  some  writers  under  the  heading  of  Constructive  or  Condensing 
Pericementitis. 

Situation. — Hypercementosis  may  be  diffused  over  almost  an  entire 
root  or  several  roots,  or  be  localized  as  a  distinct  nodule  at  some 

lateral  aspect,  or  exist  as  a  cir- 
^'^"  ^^*  cumscribed  enlargement  about  the 

apex  of  a  root,  or  at  the  neck  of 
a  root.  It  is  always  located 
where  the  cause  (hyperemia)  has 
been  produced  (Fig.  463), 

Flagg  noted  that  75  per  cent,  of 
cases  of  hypercementosis  were 
found  upon  posterior  teeth,  and 
that  the  teeth  were  usually  of  the 
character  termed  dense — i.  e.,  the 
tissues  of  the  individual  were  of  recuperative  type  tending  to  produce 
constructive  changes. 

Pathology  and  Morbid  Anatomy. — For  some  time  after  eruption  the 
cementura  consists  of  but  few  lamellae  of  deposit.  It,  however,  reaches 
a  maximum  normal  development  at  which  it  normally  rests,  as  in  the 
case  of  tlie  ])liysiological  pulp  cavity.     As  age  progresses  it  is  a])t  to 


HypercemcuLi. 


(.Skiagraph  by  Lodge.) 


IIYPERCEMENTOSIS  571 

be  more  thickly  deposited  at  the  expense  of  the  pericementum,  which 
becomes  more  attenuated.  Whether  this  is  due  to  irritants  floating 
in  the  blood  stream,  or  *o  the  various  local  irritants  above  mentioned, 
or  to  perfectly  normal  development,  is  not  clear  except  for  certain 
definite  cases. 

Nodular  and  irregular  forms  arising  from  the  general  surface  are 
clearly  of  abnormal  type. 

Successive  lamella^  are  deposited;  the  pericementum  recedes,  caus- 
ing resorption  of  the  alveolar  process.  Union  of  the  bone  and 
cementum  (ankylosis)  very  rarely  occurs.  A  resorption  of  ce  men  turn 
and  dentine  may  occur  at  some  point  owing  to  a  different  degree  of 

FiQ.  465 


^---'••:-- 
^^^"^N. 


'^^^y^. 


"^mi- 


iklVvv^ 


;;^i...^.itiii^ 


Hypertrophy  of  the  cementum  on  the  side  of  a  root  of  a  lower  molar  near  the  neck  of  the  tooth 
of  a  man:  a,  dentine;  b,  cementum;  c,  fibers  of  peridental  membrane;  from  6  to  c  the  cementum 
is  normal  and  the  incremental  lines  fairly  regular,  but  at  d  one  of  the  lameise  is  greatly  thickened; 
at  e  this  lamellse  is  seen  to  be  about  equal  in  thickness  with  the  others.  The  next  two  lamellae 
are  thin  over  the  greatest  prominence,  but  one  is  much  thickened  at  g,  and  both  at  h.  These 
latter  seem  to  partially  fill  the  valleys  which  were  occasioned  by  the  first  irregular  growth. 
From  a  lengthwise  section.     (Black.) 

irritation,  and  in  the  area  a  new  deposition  of  cementum  may  occur 
(Fig.  466,  d).  In  some  cases  distinct  areas  of  hypercementosis  and 
root  resorption  are  seen  in  close  proximity.  Chronic  apical  abscess 
may  produce  a  denudation  of  the  root  end,  and  at  a  short  distance 
below  an  annular  ridge  of  h}^ercementosis  may  occur.  Areas  of 
hypercementosis  may  be  translucent  or  decidedly  opaque,  and  some- 
times the  two  are  combined,  a  mottled  appearance  being  produced. 

If  the  growth  proximate  another  root,  the  pericementum  may  ivsorb 
at  the  point  of  contact  and  a  dejiosition  of  cementum  occur  which 
firmly  unites  the  roots  in  a  union  called  conci-escence.     (See  p.  241 .) 

It  has  occurred  that  a  root  filling  protruding  through  a  perforation 
has  caused  a  diffused  exostosis  of  the  alveolar  process.^  The  hyper- 
trophied  process  may  be  ivory-like  in  hartlness. 

'  Garretson's  Oral  Clinic,  1884. 


572 


DISEASES  OF  THE  PERICEMENTUM 


Symptoms  and  Diagnosis, — Many  cases  exist  without  active  local 
symptoms.  In  no  case  is  the  color  of  the  gum  altered  unless  other 
disease  than  h^'peremia  be  acting  as  a  cause.  In  some  cases  there  are 
symptoms  of  h^-peremia  expressed  as  a  disposition  to  bite  hard  upon 
the  particular  tooth,  or  to  grind  upon  it.  A  paroxysm  of  gnawing  pa  n 
lasting  for  some  hours,  and  recurring  at  intervals,  is  also  somewhat 

Fig.  466 


Apex  of  root  of  an  upper  bicuspid  tooth  with  irregularly  developed  cementum:  a,  a,  dentine; 
h,  b,  pulp  canals.  The  lamellae  of  cementum  are  marked  1,  2,  3,  etc.;  d,  d,  d,  absorption  areas 
that  have  been  refilled  with  cementum.  It  will  be  seen  that  the  apices  of  the  roots  were  origi- 
nally separate,  but  became  fused  with  the  deposit  of  the  second  lamella  of  cementum,  and  that 
in  this  regular  growth  began  and  was  most  pronounced.  It  has  continued  through  the  subse- 
quent lamellae,  but  in  less  degree.  It  will  also  be  noticed  that  the  absorption  areas,  d,  d,  d, 
have  proceeded  from  certain  lamellae.  That  between  the  roots  has  broken  through  the  first 
lamella  and  penetrated  the  dentine,  and  has  been  filled  with  the  deposit  of  a  second  lamella. 
Other  of  the  ab.sorptions  have  proceeded  from  lamellae  which  can  be  readily  made  out.  The 
small  points,  e,  seem  to  have  been  filled  with  the  depo.sit  of  the  last  layer  of  the  cementum, 
while  others  have  one,  two,  or  more  layers  covering  them.      (Black.) 

characteristic.  Sympathetic  hyperemia  of  the  pulp  with  increased  re- 
sponse to  thermal  changes  may  occur.  The  gum  may  have  slightly 
receded . 

Neuralgia, functional  blindness, functional  deafness,  chorea,  epilepti- 
form fits,  paralysis,  cardiac  neuralgia,  insanity,  and  other  related  con- 
ditions have  been  cured  by  the  extraction  of  hypercementosed  teeth.^ 

Th(i   treatment  of   teeth  presenting  o})stinate  symptoms  of  peri- 


'  Brubaker,  American  System  of  Dentistry. 


ANKYLOSIS  573 

cementitis,  apparently  due  to  moist  gangrene  of  the  pulp,  may  at  times 
be  complicated  by  unsuspected  hypercementosis. 

In  such  cases,  if  pulp  or  pericemental  complication  cannot  be  deter- 
mined, suspicion  should  point  to  h^-percementosis  and  an  x-ray  ex- 
amination be  made,  by  which  means  the  condition  may  be  positively 
determined.  As  entire  dentures  have  been  extracted,  tooth  by  tooth, 
in  a  vain  endeavor  to  cure  a  neuralgia  about  the  head,  this  means  of 
diagnosis  should  not  be  overlooked. 

Treatment. — The  treatment  for  hypercementosis  may  first  be  a 
conservative  one  if  only  slight  annoyance  be  produced  by  it. 

Counterirritation — correction  of  malocclusion,  etc. — may  be  em- 
ployed. The  symptoms  may  disappear.  If  they  do  not,  or  they 
are  severe  when  the  patient  applies,  the  tooth  should  be  completely 
extracted.  The  operation  of  amputation  of  the  root  end  might  be 
safely  tried  for  apical  hypercementosis,  but  there  are  no  records  of  its 
employment  as  a  means  of  cure.  The  bulbous  condition  of  the  root 
end  may  cause  extraction  to  be  difficult,  and  fracture  of  the  root  end 
may  occur.  Flagg  recommended  that  in  such  a  case  a  fissure  drill 
be  passed  about  the  circumference  of  the  root  end  to  remove  the  bony 
obstruction  to  its  passage  out  of  the  alveolus,  after  which  it  may  be 
lifted  away  with  tweezers.  Cocaine  may  be  used  as  an  obtundent. 
The  use  of  alveolar  forceps  for  the  condition  is  little  short  of  brutal, 
and  only  warranted  by  the  impracticability  of  other  means. 

Extraction  for  h^-percementosis  may  cause  considerable  bruising  of 
the  walls  of  the  alveolus,  followed  by  excruciating  pain  lasting  often 
for  days.  The  alveolus  may  refuse  to  granulate  and  a  septic  condition 
result.  The  pain  has  at  times  been  relieved  by  the  injection  of  a 
2  per  cent,  solution  of  cocaine  into  the  gum  on  either  side  of  the 
alveolus,  after  which  the  surfaces  of  the  alveolar  walls  should  be 
sterilized  and  burred  away  until  tissue  capable  of  granulation  is 
reached . 

The  alveolus  should  then  be  irrigateil  and  a  clot  invited  by  causing 
a  slight  hemorrhage.     (See  p.  553.) 

ANKYLOSIS  I  SYNOSTOSIS). 

By  this  is  meant  the  union  of  bone  and  cementum,  a  condition 
analogous  to  ankylosis  of  bone. 

Hopewell-Smith^  has  described  five  cases,  of  which  he  offers  the 

'  HistoUigy  and  Pathohistology  of  the  Teetli. 


574 


DISEASES  OF  THE  PERICEMENTUM 


following  explanation:  (1)  inflammation  occurs  and  the  membrane  is 
changed  into  granulation  tissue;  (2)  the  cellular  elements  destroy 
portions  of  the  bone  and  excavate  the  cementum;  (3)  the  mass  of 
granulation  tissue  is  then  ossified,  joining  the  bone  and  cementum  in 
a  firm  union. 

FiQ.  467 


"/ 


Vertical  section  of  a  human  tooth  ankylosed  to  the  jaw:  B,  root;  R,  bone  of  jaw.  The  abso- 
lute continuity  of  the  two  hard  tissues  is  strikingly  shown.  From  the  collection  of  the  late 
Storer  Bennett.'     (Hopewell-Smith.) 

E.  C.  Rice^  has  reported  a  case  of  a  lady  for  whom  an  implantation 
of  an  upper  bicuspid  was  done.  In  an  effort  made  later  to  remove 
the  too*^h  all  attempts  to  loosen  it  in  any  degree  with  forceps  failed. 

In  my  own  practice  an  implanted  tooth  is  firmly  immovable  in 
any  degree,  though  several  years  in  place.  The  union  may  not  be 
csseous  in  these  cases,  though  doubtless  bone  has  entered  areas  of 
previous  resorption. 

RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH. 


By  resorption  of  the  roots  of  permanent  teeth  is  meant  the  gradual 
removal  of  the  cementum  and  dentine  of  permanent  roots  by  phago- 
cytic cells  existing  in  the  adjacent  soft  tissue  (osteoclasts). 

*  Transactions  of  the  Odontological  Society  of  Great  Britain. 

*  Private  communication. 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH      575 


Causes. — The  proximate  cause  is  probably  in  all  cases  a  degree  of 
irritation  greater  than  that  required  to  produce  hypercementosis. 
Talbot's  demonstrations  of  interstitial  gingivitis,  a  term  meant  to 
include  interstitial  pericementitis,  show  that  it  is  a  frequent  cause  of 
both  root  and  alveolar  resorption.     (See  Interstitial  Gingivitis.) 

The  disease  has  been  discussed  by  other  writers  as  a  result  of 
"Rarefying  Pericementitis." 

Chronic  apical  abscess  seems  to  be  a  frequent  cause.  Although 
theoretically  the  alkaline  pus  formed  should  neutralize  acid  formation, 
the  fact  of  resorption  remains,  and  is  probably  explainable  upon  the 
ground  that  it  is  produced  by  the  granulation  tissue  formed  about 
the  root  apex  during  periods  of  lessened  pus  formation  (Fig.  447). 


Fig.  468 


Fig.  469 


Fig.  470 


Deciduous    cuspid  crowned, 

mistaken  for    permanent  cus- 

Apical       abscess      pid  which    lay    in    jaw    and 

and  resorption,  pro-     caused  resorption  of   root  of 

duced    by    a     pro-     permanent      lateral.        (Skia- 

truding  broach.  graph  by  Price.) 


Resorption  at  cervical  third  in  two 
replanted  teeth,  one  broken  in  conse- 
quence. Editor's  practice.  (Skiagraph 
by  Hagopian.) 


Protruding  root  fillings  or  broaches  are  common  causes  (Fig.  448). 
Plantations  are  frequently  followed  by  it.  A  peculiar  resorption 
in  the  cervical  third  of  two  replanted  incisors  caused  the  fracture 
of  one  at  the  point  of  resoi-ption  and  necessitated  the  removal  of 
both  teeth  (Fig.  470).  Plantations  are  usually  followed  by  peculiar 
resoiptions  over  even  the  entire  root.  liOoseness  of  a  tooth  with 
the  resultant  excess  of  movement  excites  interstitial  gingivitis.  Partial 
luxation  as  the  result  of  a  blow  or  fall  produces  the  same  result,  the 
pericementum  becoming  thickened,  the  tooth  loosened  and  extruded, 
and  malocclusion,  which  is  also  a  cause,  being  induced. 

A  toothpick  broken  off  in  the  gum  tissue  has  produced  resorption 
at  the  neck  of  the  root. 

The  descent  of  a  supernumerary  or  impacted  tooth  upon  a  per- 
manent root  has  caused  resorption,  exposing  the  pulp  of  the  resorbed 


576 


DISEASES  OF  THE  PERICEMENTUM 


root,  and  producing  pulp  reactions.  This  may  be  quite  extensive 
before  violent  symptoms  occur  (Fig.  469). 

Calculus  beneath  the  gum  margin  has  produced  resorption.  In  one 
case  noted  four  lower  incisors  presented  the  characteristic  bays  at  a 
point  one-eighth  inch  below  the  gum  Hne. 

Some  of  the  cases  exhibit  no  tangible  cause ;  the  root  resorbs  appar- 
ently as  the  result  of  a  pecuhar  reaction  upon  the  part  of  the  tissues 
of  the  individual,  who  may  lose  many  teeth  by  this  process — i.  e.,  a 
dyscrasia  exists.  The  teeth  may  be  non-carious  and  the  pulps  vital. 
In  some  of  these  cases  neurasthenia  or  a  uric  acid  diathesis  seems  to 
have  some  association  with  the  condition  (Fig.  471). 


Fig.  471 


Inflamed  ppricenipntuni,  ostfoclasts  in   llovvsliii/.s  lafim;i-.      (V.  A.  Jjatliam.) 

Pathology  and  Morbid  Anatomy. — Both  resorption  of  cementum  and 
its  redeposition  occur  in  teeth  as  physiological  processes;  at  some 
aspect  of  the  cementum  the  tissue  becomes  hollowed  out,  and  later 
filled  in  by  new  cementum.  Resorption  of  tissue  throughout  the  body 
is  'accomplished  by  means  of  multinucleated  cells  (giant  cells,  osteo- 
clasts). At  some  part  to  be  physiologically  resorb(>d  these  cells  make 
their  appearance  in  contact  with  the  tissue  to  be  removed,  and  it 
graflually  disappears,  the  layer  of  multinucleated  cells  constantly 
occupying  the  excavated  territory  known  as  Howship's  lacunae 
(Figs.  73  and  471). 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH      :,77 

If  a  foreign  (aseptic)  body  be  introduced  into  living  tissues,  it 
becomes  surrounded  by  these  cells,  which  in  some  cases  efi'ect  its 
removal;  in  others,  failing  to  remove  the  foreign  body,  connective 
tissue  forms  about  it  and  encysts  it;  encystment  may  occur  after 
partial  removal  by  giant  cells. 

The  resor})tion  may  be  of  any  extent,  from  a  slight  spicnlar 
roughness  of  the  apex  of  the  root  to  almost  complete  removal  of  the 
root. 

Perforation  of  the  root  from  side  to  side  may  occur,  of  course, 
involving  the  pulp  canal,  and,  if  the  pulp  be  alive,  obscure  reactions 
upon  its  part  may  occur  (Fig.  472). 

An  area  of  marked  resorption  may  occur  at  a  point  just  beneath 
the  gum  margin  and  upon  any  aspect  of  the  tooth.     In  this  situation 
it  may  simulate  a  cavity  of  decay  beneath  the  gum.     It  occurs  upon 
either  vital  or  devitalized  teeth,  and  may  expose 
the  pulp  or  the  root-canal  filling.     The  gum  ^^^-  ^^^ 

tissue  is  usually  found  within  the  cavity. 

It  is  probable  that  in  plantations  the  root 
acts  as  an  aseptic  foreign  body;  mild  inflam- 
mation occurs,  subsides,  and  giant  multinu- 
cleated cells  attack  the  tooth  root  and  endeavor 
to  remove  it  by  solution;  this  they  accomplish, 
in  part,  in  spots;  then  a  tolerance  is  established  peJ^iZrn^rUr'C bay 
and  connective  tissue  organizes  about  the  roots;     "p""  t''^  ^^^^  exposed  the 

,  ,  .  .  !>ulp    and    perforated    the 

later,  more  complete  regeneration  is  represented     root  as  shown.   Crater-iike 
in  the  formation  of  bone;  a  condition  of  bony     ^sorption    about    apical 

•'        foramen.     Pulp  first  devi- 

fixation  is  established,  evidenced  by  the  clear-     taiized  on  account  of  per- 

,         !•    ..     1  ,  •  ,1  1  1       sistent  pain  and  the  tooth 

ringing  note  elicited  upon  tapping  the  planted     i^ter  extracted, 
tooth. 

With  reference  to  resorption  after  plantations,  INIiller^  records  tlu^ 
following  results  of  his  observations.  The  fixation  of  reimplanted  or 
transplanted  teeth  may  be  accomplished  in  three  ways: 

1.  By  simple  encapsulation  of  the  root. 

2.  By  the  bundles  of  connective  tissue  which  fill  up  irregular 
absorption  spaces,  especially  where  the  pericementum  has  not  been 
present  at  that  portion  when  the  implantation  was  made  (a  pseudo 
attachment). 

3.  By  direct  union  of  the  surrounding  tissues  with  the  living  peri- 
cementum.    He  inclines  to  think  this  the  only  permanent  attachment. 

'  Independent  Practitioner,  1887. 

37 


578 


DISEASES  OF  THE  PERICEMENTUM 


He  states  that  for  the  most  part  osteoclasts  were  few  and  that 
resorption  was  carried  on  by  small  round  cells. 

The  inflammatory  reaction  and  resorption  is  least  when  replantation 
is  practised,  but  may  at  times  be  pronounced  in  even  those  cases.  If 
the  socket  of  a  tooth  extracted  for  resorption  be  examined,  a  mass  of 
soft  tissue  will  be  found  occupying  the  locations  corresponding  to  the 
areas  of  resorption  (Fig.  473).  No  acid  reaction  can  be  detected  with 
litmus  paper,  but,  nevertheless,  it  is  probable  that  the  cells  producing 
resorption  excrete  an  acid  capable  of  dissolving  the  tissue. 

There  is  some  evidence  of  this  in  cases  of  enamel  resorption  occur- 
ring upon  the  crowns  of  impacted  teeth  which  have  never  been  in 
relation  with  the  oral  fluids,  and  about  which  there  is  no  evidence  of 
caries  in  the  areas  of  dentine  resorption  also  present.  In  the  fortunate 
specimens  of  these  cases  a  superficial  decalcification  of  the  enamel 
surface  may  be  seen  which  can  only  occur  as  the  result  of  acid  action. 


Fia.  473 


Fig.   474 


Resorption  of  distal  root  of  a  first  molar. 
(Skiagraph  by  Custer.) 


Diagram  of  a  case  of  root  resorption  after 
secondary  dentine  had  formed:  SD,  secondary 
dentine;  AR,  area  undergoing  resorption; 
peculiar  central  spire  of  secondary  dentine 
which  has  resisted  the  resorbent  action. 
Specimen  in  possession  of   Dr.  A.  P.  Fellows. 


Symptoms  and  Diagnosis .^ — The  tooth  may  present  symptoms  of 
iion-scptic  pericementitis,  and  may  be  loosened  in  advanced  cases. 
In  the  early  stages  no  looseness  may  be  observed  until  a  strain  suddenly 
aj)plied  causes  a  luxation;  thereafter  the  tooth  progressively  loosens. 

The  condition  may  be  discovered  by  accident:  evidences  of  mild 
pericementitis  appear,  and  the  pulp  canal  is  opened  to  search  for  a 
cause.  The  pulp  may  be  found  alive;  if  alive,  and  it  is  killed,  or  if  it 
is  found  dead,  broaches  pass  suddenly  into  the  mass  of  soft  tissue 
midcrlying  the  root.  The  progressive  loosening  of  the  tooth,  with 
its  pecuHar  movement,  is  about  the  only  constant  symptom  of  the 
condition. 

In  cases  of  live  pulp  this  organ  may  be  hyperemic,  so  that  inci'eased 
respon.sc  to  heat  or  cold  is  felt;  this,  taken  in  connection  with  the 


DEGENERATION  OF  THE  PERICEMENTUM  570 

teiuk-riu'ss  upon  percussion  which  can  usually  be  elicited,  and  with 
the  peculiar  loosening  of  the  tooth,  is  a  diagnostic  guide. 

Flagg^  stated  that  reflex  neuralgias  occur  in  this  condition,  but  that 
the  most  constant  indication  noted  by  him  was  a  sense  of  discomfort 
about  the  jaws,  vaguely  associated  with  some  one  tooth.  The  patient 
is  convinced  that  if  the  tooth  were  removed  relief  would  follow.  In 
the  absence  of  the  loosening,  which  may  not  occur  until  the  root  is 
nearly  gone,  the  resorption  is  most  commonly  discovered  by  entering 
the  pulp  canal  and  finding  its  length  much  shoitened.  In  some  cases 
the  resorption  may  be  found  near  the  gum  margin  and  simulating  a 
cavity  of  decay,  from  which  it  may  readily  be  diagnosticated  by  its 
appearance  when  exposed  by  packing  the  gum  away.  Such  cases 
appear  to  accompany  a  marginal  gum  resorption. 

The  a'-rays  should  exhibit  the  condition  with  sufficient  clearness  to 
furnish  an  absolute  diagnosis. 

If  a  direct  diagnosis  can  be  made,  the  tooth  should  be  extracted, 
except  in  the  cases  near  the  gum  margin,  which  may  be  filled  usually 
with  plastic  fillings.  If  a  diagnosis  be  not  possible,  probable  causes  of 
irritation  should  be  sought  for  and  removed  and  the  non-septic  peri- 
cementitis treated  as  indicated.     (See  p.  566.) 

Failing  a  cure,  the  tooth  is  to  be  removed,  when  a  jiost  hoc  diagnosis 
may  be  made.  In  view  of  the  availability  of  the  a'-rays  this  involves 
an  unnecessary  endurance  and  loss  of  time. 


DEGENERATION  OF  THE  PERICEMENTUM. 

Strictly  speaking,  the  overuse,  abuse,  and  disuse  of  the  tee'th  are 
causes  which  produce  a  general  hyperemia  or  inflammation  of  the 
pericementum  (non-septic  pericementitis).  If  continued,  the  inflam- 
mation extends  into  the  gum  tissue  and  an  interstitial  gingivitis  is 
produced.  The  results  of  the  causes  are,  therefore,  classifiable  under 
either  non-septic  pericementitis  or  interstitial  gingivitis.  Either  of 
these  conditions  renders  the  tissues  involved  liable  to  the  degenerations 
and  resorptions  which  accompany  continued  hyperemia  or  inflamma- 
tion, or  acts  as  a  predisposing  cause  to  local  infection  by  oral  organisms, 
beginning  its  action  at  the  gum  margin,  and  which  sooner  or  later 
produces  a  purulent  liquefaction  of  the  gingival  portion  of  the  peri- 
cementum (pyorrhea  alveolaris). 

'  Lectures  on  Dentel  Therapeutics. 


580  DISEASES  OF  THE  PERICEMENTUM 

In  view  of  applied  therapeutics  it  is  well  to  consider  these  causes 
separately. 

OVERUSE  OF  TEETH. 

Bv  overuse  of  a  tooth  is  meant  such  a  variety  of  occlusion  that  the 
tooth  receives  a  greater  stress  than  its  neighbors,  or  than  it  is  designed 
to  bear.  The  stress  may  be  received  in  the  normal  direction  but  be 
excessive  in  amount.  The  most  prominent  cause  of  this  condition  is 
the  loss  of  one  or  more  other  teeth,  permitting  undue  stress  to  fall  upon 
the  neighboring  teeth,  or,  in  some  cases,  on  far-distant  teeth.  Too 
prominent  artificial  crowns,  particularly  those  of  the  all-gold  type, 
cause  a  general  increase  of  stress  upon  the  pericementum.  Enormous 
overfull  contour  fillings  may  establish  a  similar  condition.  When  but 
few  isolated  teeth  remain  in  one  denture  and  have  antagonists,  the 
teeth  are  certain  to  be  overworked.  Isolated  and  other  teeth  to  which 
are  attached  clasps  of  artificial  dentures  or  too  large  pieces  of  bridge 
work,  are  in  the  majority  of  cases  being  constantly  overstrained. 

Pathology. — Like  any  other  functional  part  which  is  overworked, 
the  pericementum  is  first  stimulated,  causing  the  vessels  to  dilate. 
Soon  evidences  of  overwork  appear,  and  the  condition  passes  into 
one  of  interstitial  pericementitis;  the  tooth  projects,  and  is  loosened; 
the  overlying  gum  deepens  in  color,  and  evidences  of  venous  engorge- 
ment are  common  (interstitial  gingivitis).  The  result  of  the  condition, 
is  a  softening  and  degeneration  of  the  substance  of  the  pericementum; 
the  alveolar  wall  is  involved  in  the  degeneration,  and  it  melts  down^ — 
is  resorbed  to  a  greater  or  less  extent.  At  any  stage  of  the  disturbance 
infection  may  occur,  and  the  degeneration  and  destruction  of  the 
pericementum  be  hastened  by  suppuration  or  other  secondary  degen- 
erations. 

The  symptoms,  diagnosis,  and  clinical  history  are  involved  in  the 
description.  The  prognosis  is  the  inevitable  loss  of  the  tooth  if  the 
causes  be  not  removed,  in  which  event  the  prognosis  is  governed  by 
the  extent  to  which  the  degeneration  has  proceeded.  (See  Interstitial 
Gingivitis.)  These  cases  are  often  seen  at  a  time  when  it  is  difficult  to 
say  which  came  first,  the  pyorrhea  or  the  overwork,  but  the  conditions 
of  evident  overstrain,  as  when  posterior  occlusion  is  largely  lost,  and 
the  usually  prompt  response  to  surgical  rest  lead  to  inference  that 
overwork  started  the  predisposition  to  pyorrhea. 

'i'he  teeth,  if  in  ovcrocc.-lusion,  should  be  dressed  ott"  until  properly 


MALOCCLUSION  OF  THE  TEETH  581 

occluded.  Prosthetic  appliances  shoidd  not  be  so  attached  by  clasps 
as  to  unduly  move  the  clasp  teeth,  especially  buccolingually.  The 
U-clasp  is  worthy  of  consideration  in  this  regard.  The  appliance 
should  support  the  teeth  laterally,  if  possible,  and  occasionally  the 
enclosure  of  the  teeth  by  the  plate  clasps,  with  the  hooks  facing  each 
other  or  a  buccal  embracing  wire  stay,  is  rec|uired,  as,  for  example, 
where  four  lower  bicuspids  only  are  retained  for  support  to  the  plate, 
yet  where  they  also  require  support.  No  attempt  is  made,  however,  to 
cause  the  artificial  teeth  to  strike  before  the  natural  teeth,  in  the  hope 
of  giving  surgical  rest  to  these  organs.  Such  attempts  always  result  in 
failure,  as  they  cause  injuries  to  the  tissues  upon  which  the  plate  and 
teeth  rest,  which  are  more  severe  than  the  pericemental  disturbance. 

Properly  adjusted  bridge-work  frequently  does  goofl  service  in  these 
cases,  provided  the  overoccluding  tooth  or  teeth  be  first  dressed  down 
short  of  occlusion  and  are  given  a  period  of  rest  until  the  peri- 
cementum recovers.  The  bridge,  if  carefully  planned,  may  be  made 
to  direct  and  control  the  stress  received  by  the  injured  teeth.  In  this 
connection  what  is  termed  the  "overarch  bar"  is  a  valuable  device, 
as  it  automatically  throws  some  of  the  stress  received  by  the  diseased 
teeth  upon  teeth  upon  the  other  side  of  the  arch,  which  naturally  are 
forced  in  an  opposite  direction  during  mastication. 

Improperly  occluding  artificial  crowns  should  have  this  fault 
corrected  by  removing  the  excess  of  material  or  by  setting  properly 
made  crowns. 

Overfull  fillings  shoukl  be  reduced  to  correct  proportions  and  shape. 

Surgical  rest  is  the  only  hope  of  saving  the  tooth. 

MALOCCLUSION  OF  THE  TEETH. 

Each  tooth  of  a  denture  is  not  only  designed  to  receive  a  definite 
amount  of  force,  but  to  receive  it  in  a  particular  direction  or  directions; 
any  excess  of  this  force,  or  alteration  of  its  direction,  is  followed  by 
abnormal  stimulation  of  the  pericementum  and  by  its  overstraining. 
The  efi'ects  following  a  general  increase  of  stress  have  been  considered 
under  the  previous  heading.  By  malocclusion  is  here  meant  the 
constant  reception  of  stress  by  the  pericementum  in  directions  to 
which  it  is  (piite  unaccustomed,  or  are  not  in  accordance  with  the 
anatomical  design  of  the  tooth.     It  is  a  peculiar  form  of  overuse. 

Causes. — Original  malpositions  of  the  teeth  may  cause  their  faulty 
occlusion.     The  most  prolific  source  of  the  condition   is,  however, 


582  DISEASES  OF  THE  PERICEMENTUM 

altered  occlusion  clue  to  those  changes  of  position  of  the  teeth  which 
follow  upon  the  loss  of  adjoining  teeth. 

Artificial  croT^Tis,  which  do  not  occlude  in  correspondence  with  the 
other  teeth,  are  a  common  cause.  Improperly  formed  fillings  are 
another  cause. 

The  shifting  of  positions  of  the  teeth,  in  consequence  of  pathological 
changes  occurring  in  or  about  the  pericementum,  causes  the  crowns  of 
teeth  to  occlude  improperly. 

Pathology. — The  conditions  established  are  those  of  overuse  in  a 
direction  other  than  direct.  A  typical  example  of  this  condition  is  that 
of  a  lower  second  molar  which  has  gradually  tilted  forward  in  conse- 
quence of  the  loss  of  the  first  molar;  or  a  central  incisor  which  has 
altered  its  position  in  consequence  of  secondary  formations  in  or  about 
the  pericementum,  a  common  precursor  of  phagedenic  pericementitis. 
Some  portion  of  the  tooth,  an  edge,  which  before  did  not  occlude  with 
an  antagonizing  tooth,  is  brought  into  occlusion;  if  the  occlusion  be 
not  unduly  forcible,  no  immediate  degenerative  changes  are  evident. 
If  the  occlusion  be  excessive,  the  pericementum  is  not  uniformly 
affected,  but  the  greatest  stress  is  brought  to  bear  upon  some  lateral 
aspect  of  the  structure.  It  responds  in  the  degree  of  the  overwork, 
and  degenerative  changes  occur,  which,  if  the  active  causes  be  not 
removed,  gradually  spread  to  other  portions  of  the  pericementum,  and 
the  phenomena  noted  in  connection  with  overuse  occur,  but  are  not 
so  general  in  distribution.  The  tooth  becomes  more  movable  in  one 
or  more  directions — i.  e.,  is  loosened;  it  may  develop  some  degree  of 
tenderness  upon  percussion,  and  the  gum  color  toward  the  affected 
side  deepens,  although  it  may  remain  normal  in  other  parts.  As  in 
the  previous  cases,  infection  may — indeed,  is  likely  to — occur.  In 
some  cases  the  pericementum  may  degenerate  and  be  destroyed  about 
one  root  of  a  multi-rooted  tooth,  and  remain  about  the  other.  It  is 
to  be  remembered  that  a  less  degree  of  irritation  may  produce  hyper- 
cementosis. 

Pyorrhea  alveolaris  in  any  form  is  a  localized  suppurative  peri- 
cemental inflammation,  with  which  the  pericementum  in  general  or 
even  the  pulp  sympathizes  in  a  general  hyperemia  or  even  in- 
flammation. Swelling  occurs  and  the  tooth  is  pushed  up  into  mal- 
occlusion. Such  teeth  may  sometimes  be  dressed  off  one-thirty- 
second  of  an  inch  before  the  overocchision  is  relieved.  A  direct  result 
of  the  strain  and  compression  brought  to  bear  upon  apical  tissue  is 
the  production  of  non-septic  pulpitis  with  reflex  pain  and  response  to 
heat  and  cold. 


DISUSE  OF  TEETH  583 

Diagnosis  and  Treatment. — In  all  malposed  teeth  a  careful  examina- 
tion slioukl  be  made  of  their  mode  of  occlusion.  If  tiie  tooth  exhil)it 
tenderness  and  looseness,  malocclusion  is  almost  a  certainty;  it  only 
remains  to  determine  its  direction. 

The  spots  of  faulty  occlusion  may  be  determined  by  placing  a  strip 
of  carbon  paper  (articulating  paper)  over  the  tips  of  the  antagonizing 
teeth  and  having  the  patient  bite;  the  spots  of  contact  should  tlien 
be  ground  away  until  the  tooth  is  slightly  short  of  direct  occlusion. 
Fresh  strips  of  paper  are  used,  and  the  jaws  moved  laterally,  as  in 
mastication,  to  note  other  points  of  contact;  these  should  also  be 
ground  away. 

It  suffices  in  some  acute  cases  to  place  a  rubber  dam  or  metal  caj) 
guard  upon  a  nearby  tooth  for  a  day  or  two  to  prevent  occlusion  u])()n 
the  sore  tooth,  which  regains  its  normal  position  in  the  alveolus  as 
the  inflammation  subsides.  The  grinding  and  guarding  may  he 
combined,  judgment  being  required. 

Prognosis. — If  the  condition  be  not  corrected  every  time  occasion 
requires,  the  degeneration  progresses  until  the  tooth  is  lost. 

If  marginal  infection  have  occurred,  purulent  or  non-purulent  mar- 
ginal pericemental  liquefaction  (pyorrhea  alveolaris)  may  have  to  be 
considered. 

DISUSE  OF  TEETH. 

Definition. — Bv  disuse  of  teeth  is  meant  a  decree  of  usajre  less  tlian 
the  amount,  the  forms,  and  structure  of  the  teeth  and  contiguous  parts 
fit  them  for.  Tlie  disuse  may  be  absolute  or  relative;  teeth  may  not 
occlude  at  all,  owing  to  the  loss  of  antagonists  or  to  extremely  irregular 
positions. 

Partial  Disuse.— Causes  and  Pathology. — If  soft  food  be  u.sed 
insteatl  of  that  requiring  vigorous  mastication,  or  if  one  tooth  of  a 
side  be  diseased  so  tliat  that  side  of  the  mouth  is  unused  in  mastica- 
tion, or  if  one  of  the  antagonists  of  a  tooth  be  lost,  the  pericenienti  of 
the  teeth  involved  do  not  receive  their  ])roj)er  amount  of  exercise,  and 
a  degree  of  atony  ensues. 

This  partial  disuse  has  a  more  distinct  relation  to  the  health  of  the 
gum  margin,  which  does  not  receive  a  normal  amount  of  friction 
from  mastication,  and  if  this  be  not  offset,  in  part,  by  proj)hylaxis, 
marginal  gingivitis  ensues. 

Infection  and  the  formation  of  calculus  increase  the  irritation  to  a 


584  DISEASES  OF  THE  PERICEMENTUM 

marginal  gum  inflammation,  which  is  hable  to  run  into  a  pyorrhea 
alveolaris.     This  is  the  real  significance  of  disuse  as  a  cause. 

Diagnosis  and  Prognosis. — A  diagnosis  of  disuse  (relative)  is  usually 
made  out  by  inquiring  as  to  the  food  habit  of  individuals.  It  is 
excessively  common  in  civilized  communities,  particularly  among  the 
well-to-do,  and  is  of  almost  constant  occurrence  in  gourmands. 

Treatment. — Patients  should  have  pointed  out  to  them  the  results 
of  insufficient  mastication,  together  with  the  evils  of  faulty  oral  hygiene. 
Every  effort  should  be  made,  by  the  use  of  constant  prophylactic 
measures,  to  forestall  the  occurrence  of  pyorrhea  alveolaris.  This 
and  similar  conditions  are  particularly  to  be  feared  in  the  degenerative 
periods  of  early  and  late  middle  age.  It  is  between  the  ages  of  thirty 
and  fifty  years  that  ill-consequences  are  most  to  be  feared  from 
acquired  debility  of  the  pericementum. 

Absolute  Disuse. — Teeth  which  perform  no  work  directly  in 
mastication,  or  indirectly  by  serving  as  abutments  for  a  bridge-piece, 
may  be  said  to  be  in  a  condition  of  absolute  disuse. 

Results. — ^A  tooth  or  root  whose  pericementum  receives  no  stimulus 
becomes  relatively  a  foreign  body  to  the  organism.  It  is  a  useless  part, 
and  the  body  attempts  to  cast  it  out.  Perhaps  these  phases  are  insuf- 
ficiently exact;  however,  a  disused  tooth  is  lost  through  a  series  of 
pathological  changes.  Teeth  which  perform  no  work  may  be  retained 
in  the  mouths  of  young  adults  for  long  periods  without  marked 
changes  occurring  in  their  vital  connections,  but  during  the  degen- 
erative period  of  life  they  are  usually  lost  with  a  degree  of  rapidity 
differing  in  individuals. 

The  pericementum  is  irritated  and  swells  slightly,  extruding  the  tooth. 
This  is  a  fairly  rapid  process,  and  occurs  often  after  the  trimming  of 
teeth  for  bridge-work  so  as  to  interfere  with  the  bite,  unless  the  bridge 
be  rapidly  made.  If  unopposed,  it  extends  progressively,  the  neck 
being  usually  exposed,  though  sometimes  the  alveolar  process  becomes 
developed  and  lies  on  a  lower  level  as  though  it  had  followed  the  tooth 
down.  Usually  the  bifurcation  of  a  molar  becomes  exposed,  calculi 
form,  and  the  extrusion  becomes  hastened  by  marginal  gingivitis. 
The  tooth  may  be  firm,  even  though  half  its  root  length  be  exposed, 
though  often  it  becomes  looser  than  normal.  Sometimes  it  strikes 
other  teeth  with  a  glancing  motion.  If  the  teeth  in  Fig.  475  were 
closer  this  would  occur,  and  such  a  process  (malocclusion)  hastens  the 
loosening.  The  opposite  gum  may  be  injured  by  such  a  tooth. 
Another  effect  is  the  wedgiuK  <>f  food  })etween  the  teeth  owing  to  a 


DISUSE  OF  TEETH  585 

favoring  entrance,  the  laterally  unsupported  tooth  wedging  apart  and 
then  closing  upon  the  food. 

Finally  the  loosening  or  the  annoyance  compels  the  removal  of  the 
tooth. 

The  danger  of  marginal  infection  is  always  great  in  these  cases. 
Some  degree  of  infection,  no  doubt,  exists  in  all  of  them,  which  serves 
to  explain  the  increased  rapidity  of  the  degenerations. 

Prognosis. — If  teeth  can  be  directly  or  indirectly  brought  into  use, 
so  that  their  pericementi  receive  exercise,  the  cases  may  recover,  pro- 
vided the  atrophic  changes  are  not  very  pronounced;  in  which  event 
the  atrophy  proceeds,  although  more  slowly.  Teeth  crowned  or  made 
abutments  for  bridges,  after  tlegenerative  changes  have  become  estab- 

FiG.  475 


Absolute  disuse   and   elongation  of   an  ujtper  and  a  lower  molar;   partial  disuse  of   bicuspid; 
small  abscess  cavity  in  the  hone  about  a  root.      (Philadelphia  Dental  College  Museum.) 

lished — i.  e.,  when  the  normal  pericementum  has  been  replaced  by 
a  thickened  mass  of  partially  organized  connective  tissue — lusually 
become  progressively  looser;  the  alveolar  atrophy  proceeds  until  all 
attachment  is  lost. 

If  this  principle  be  utilized  early,  the  teeth  may  be  saved.  The 
results  are  better  if  the  teeth  or  roots  be  utilized  before  the  age  of 
thirty  than  at  later  ages. 

Treatment. — The  treatment,  as  might  be  inferred  from  the  foregoing 
statements,  consists  in  bringing  the  teeth  into  use,  if  the  degeneration 
have  not  proceeded  too  far.  In  crowning  for  a  bridge  pier  it  is 
customary  to  shorten  the  crown  to  the  general  occlusal  level,  though 
even  if  a  little  lono-er  and  not  in  direct  occlusion  tlio  tooth  is  broujrht 


586 


DISEASES  OF  THE  PERICEMENTUM 


into  a  sort  of  mastication  which  is  useful  if  it  does  not  introduce  an 
element  of  malocclusion,  i.  e.,  if  the  distal  or  repelling  strain  upon  its 
mesial  slope  is  compensated  for  by  the  mesial  strain  upon  a  pier  or 
piers  more  mesial  to  it;  for  example,  upon  the  cuspid  of  Fig.  475. 
In  such  a  case  as  this  grinding  both  the  upper  and  lower  molar  occlu- 
sally  and  the  introduction  of  an  upper  bridge  is  indicated.  Later, 
extraction  is  inevitable.  The  operation,  when  determined  upon, 
should  not  be  delayed,  for  not  only  are  bacterial  growths  invited  about 
the  loosened  tooth,  but  the  soft  tissues  are  frequently  increased  in 
volume,  and  if  extraction  be  delayed  until  complete  local  atrophy  of 
the  alveolar  walls  has  taken  place,  a  soft  and  spongy  mass  remains, 
which  interferes  with  the  comfortable  wearing  of  prosthetic  appliances 
in  the  future. 

FIBROID  DEGENERATION  OF  THE  PERICEMENTUM. 

Fibroid  degeneration  of  the  pericementum  is  a  senile  atrophic  change 
occurring  in  teeth,  the  pericementi  of  which  have  run  a  healthy  life 

Fig.  476 


^x>^^*/ 


^Ik^JMf 


Fibroid  degeneration  of  the  pericemeutum :  C,  cementum;  A,  alveolus;  /'',  fibers  with  decrepit 
nuclei.     Transverse  section.     (Hopewell-Smith.) 


FIBROID  DEGENERATION  OF  THE  PERICEMENTUM       587 

course,  but  finally  have  become  subject  to  senile  marantic  consti- 
tutional changes  of  not  clear  nature.  The  condition  thus  first  defined 
by  Hopewell-Smith^  is  further  described  as  found  in  that  class  of 
teeth  of  the  aged  which  have  resorbed  alveolar  margins  and  exposed 
cementum,  but  not  necessarily  subject  to  pyorrhea  alveolaris;  though 
traumatic  pericementitis  may  be  present.  In  some  cases  the  teeth 
may  be  firm. 

Fig.  477 


H 


—  M 


Fibroid  degeneration  of  the  pericementum:  C,  cementum;  M,  degenerated  pericementum; 
A,  alveolus;  //,  enlarged  (osteoporous)  Haversian  canals.  Transverse  section.  (Ho|jewell- 
Smith.) 

Pathohistology. — The  chief  characteristics  are  an  increase  in  size 
of  the  fibers  of  the  pericementum,  the  loss  of  their  nuclei,  their 
generally  structureless  character,  and  their  arrangement  in  prominent 
bundles  al)out  large  spaces  (areola^).     (See  Fig.  47(5.) 

The  fibers  are  firmly  implanted  in  both  bone  and  cementum.  The 
cementum  does  not  become  hyperplastic  (hypercementosed),  but  the 
bone  becomes  osteoporous  and  the  Haversian  canals  contain  a 
shrunken  fibroid  tissue  resembling  that  in  the  pericementum  (Fig. 
477). 


'  Dental  Cosmos.  1904. 


588  DISEASES  OF  THE  PERICEMENTUM 

The  gum  tissue  in  the  vicinity  also  undergoes  retrogressive  changes 
in  sympathy,  becomes  less  vascular  and  more  fibroid. 

The  condition  may  persist  without  inflammatory  or  suppurative 
changes,  though  it  may  act  as  a  cause  of  obscure  neuralgia  or  as  a 
predisposing  cause  to  pyorrhea  alveolaris. 

Hopewell-Smith  points  out  that  the  areolar  spaces  may  admit  micro- 
organisms to  deep  parts,  thus  predisposing  to  antral  disease  or, 
possibly,  osteomyelitis. 


ACCIDENTS  TO  TEETH. 

Apart  from  fracture  of  the  teeth  by  accidents,  several  interesting 
accidental  conditions  involving  therapeutics  require  consideration. 

Teeth  Driven  into  Alveolar  Process. — Blows,  falls,  etc.,  have 
occasionally  caused  teeth  to  be  driven  forcibly  into  the  jaw.  The 
condition  may  be  complicated  by  fracture,  in  which  case  the  judg- 
ment of  the  operator  must  be  exercised.  If  the  tooth  be  not  fractured 
it  may  be  drawn  down  with  forceps  and  ligated  in  place  until  firm. 
The  use  of  zinc  phosphate  upon  the  ligatures,  if  possible  to  use  it, 
renders  them  more  rigid.  If  evidence  of  pulp  death  be  noted  by 
subsequent  test,  or  apical  pericemental  inflammation,  the  pulp 
should  be  removed. 

Luxation  or  Partial  Dislocation  by  Accident. — Teeth  may  be 
partially  knocked  out  and  driven  either  lingually  or  buccally.  The 
pulp  connections  will  be  ruptured,  as  a  rule,  but  after  asepsis  of  the 
parts  by  means  of  antiseptic  sprays  the  teeth  may  be  pressed  into  place, 
and  if  ligated  or  splinted  may  again  become  firm  by  deposition  of 
bone  about  them.  The  pulps  nearly  always  give  evidence  of  death; 
so  that  they  should  be  later  replaced  by  canal  fillings. 

Mendel  Joseph  and  Dassonville^  record  experiments  on  dogs 
showing  a  vital  attachment  of  the  pulp  of  an  immediately  replanted 
tooth.     They  used  strictly  aseptic  precautions. 

Occasionally  evidences  of  reattachment  of  pulp  have  been  recorded, ^ 
even  after  total  displacement.  If  the  accident  result  in  elongation  of 
the  tooth  with  production  of  a  chronically  spongy  pericementum, 
the  operation  of  replantation  should  be  performed. 

Total  Dislocation  of  Teeth  by  Accident. — If  the  accident  result  in 
total  displacement  from  the  mouth,  the  tooth  or  teeth  may  be  prepared 

'  L'(Jdoiitologi(!.     See  iJerital  Cosmos,  190(>,  p.  1000.  ^  Kirk  and  W.  I'nipman. 


ACCIDENTS  TO  TEETH  589 

as  for  replantation  (see  p.  549),  and  under  aseptic  precautions  re- 
planted in  their  alveoli.  If  held  by  ligatures  or  splints  they  will 
usually  become  firm. 

Attachment  of  Teeth. — Two  or  more  teeth  may  be  attached  by  the 
intervening  alveolar  process,  fracture  of  which  may  cause  both  teeth 
to  be  removed  in  extraction.  In  a  few  cases  of  loose  deciduous  teeth 
the  gum  has  been  sufficient  attachment  to  cause  the  removal  of  two 
teeth  at  once. 

In  some  cases  the  tough,  fibrous  nature  of  the  pericementum  causes 
the  alveolar  bone  fractured  by  the  leverage  upon  it  to  remain  attached 
to  the  tooth,  and  Fig.  183  illustrates  teeth  attached  by  union  of  peri- 
cementum only. 

Fracture  of  the  Alveolar  Process.— Slight  fractures  of  the 
alveolar  plate  are  of  little  consequence,  as  a  rule.  In  some  cases  one 
plate  may  be  fractured,  and,  unless  removed  with  the  tooth,  may 
usually  be  pressed  back  into  place.  Reunion  may  be  looked  for  if 
asepsis  be  maintained.  Fractures  of  the  alveolar  process  from  blows, 
kicks,  etc.,  upon  the  jaw  may  become  septic  and  sequestra  may  form, 
necessitating  removal  of  both  bone  and  teeth.  Such  fractures  should 
have  immediate  attention.  Fractures  of  the  maxillae  should,  of  course, 
be  immediately  reduced. 

Hemorrhage  Following  Extraction.— Even  in  the  absence  of 
hemophilia  postextraction  hemorrhage  may  be  somewhat  severe,  and 
is  well  controlled  by  a  little  tannic  acid  or  powdered  alum  and 
thymol  upon  a  pellet  of  cotton,  or  nosophen  gauze  w^et  with  phenol- 
sodique. 

If  necessary  a  linen  compress  should  be  placed  over  it  and  a  Barton 
or  Garretson  bandage  applied.  The  internal  use  of  calcium  chloride 
or  other  hemostatic  is  indicated  if  the  bleeding  be  continued. 
(See  p.  111.) 

Lacerations. — The  tongue,  floor  of  the  mouth,  etc.,  may  be 
lacerated  by  the  careless  use  of  forceps,  and  the  lacerated  parts 
should  be  irrigated  with  antiseptics  and  the  mouth  kept  under 
astringent  antiseptics  while  the  parts  are  healing. 

Postextraction  Alveolitis.— This  has  been  already  discussed. 
(See  p.  553.) 

For  ordinary  transient  pain  phenol  camphor  with  or  without 
menthol  added,  or  equal  parts  of  phenol-sodique  and  laudanum  are 
useful. 


SECTION   VI. 

PERICEMENTAL  DISEASES  BEGINNING  AT 
THE  GUM  MARGIN 


CHAPTER   XXIl. 

Nearly  all  the  degenerations  of  the  pericementum,  which  begin 
at  the  gum  margin,  are  sooner  or  later  accompanied  by  suppurative 
processes,  which  give  a  generic  name  to  these  conditions,  viz.,  pyor- 
rhea alveolaris.  Under  this  head  dental  writers  have  included  several 
disease  processes  which  should  be  clearly  differentiated  from  one 
another.  In  general  terms  these  diseases  are  characterized  by  an 
inflammation  originating  about  the  gum  margin,  and  followed  by  a 
progressive  degeneration  and  atrophy  of  the  pericementum  and  of  the 
alveolar  walls.  In  the  areas  of  pericemental  atrophy  and  death  pro- 
gressive deposits  of  calculi  take  place,  and  infection  of  the  diseased 
territory  by  pyogenic  organisms  is  frequent.  Their  characteristics, 
therefore,  are  loss  of  pericementum  in  any  direction,  forming  pockets 
in  which  calculi  deposit,  and  from  which  pus  exudes  or  may  be  pressed. 
The  primary  cause  of  the  atrophy,  pericemental  necrosis,  calculi,  and 
infection  are  so  clearly  associated  with  a  primary  affection  of  the 
gums  about  the  necks  of  the  teeth,  that  a  critical  examination  of  the 
causes,  clinical  history,  and  pathology  of  inflammation  of  the  gum 
margin  is  a  necessary  preliminary  to  the  study  of  the  later  degen- 
erations. 

GINGIVITIS. 

By  gingivitis  is  meant  an  inflammation  of  the  gum.  W  hen  dislinetly 
confined  to  the  gum  margin  it  may  be  designated  as  marginal  gingi- 
vitis. When  the  inflammation  has  reached  the  deeper  connective 
tissues  of  the  gum  and  pericementum  it  has  been  culled  interstitial 
gingivitis  (Talbot).  Strictly  speaking  all  inflammations  are  inter- 
stitial, but  the  division  is  warrantable. 


592     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 


MARGINAL  GINGIVITIS. 

Definition. — By  marginal  gingivitis  is  meant  an  inflammation  con- 
fined to  the  margins  of  the  gums  about  the  necks  of  the  teeth. 

Causes. — The  causes  of  marginal  gingivitis  are  local  and  general, 
which  may  be  subdivided  into  predisposing  and  exciting.  Both  local 
and  general  causes  may  be  in  action  at  the  same  time. 

Local  Causes. — Marginal  gingivitis  may  be  excited  by  the  pres- 
ence of  food  masses  or  unremoved  collections  about  the  necks  of  teeth, 
their  fermentation  liberating  chemical  products  more  or  less  irritating. 
Miller^  has  shown  that  the  materies  alba  about  the  necks  of  teeth 
may  have  either  an  alkaline  or  acid  reaction  and  the  gums  be  in- 
flamed. 

Bacterial  plaques  not  unlike  those  producing  dental  caries  have 
been  shown  by  Miller^  to  be  formed  upon  many  surfaces  of  the  teeth 
even  when  no  ill  results  are  notable.  In  practice  staining  the  teeth 
with  tincture  of  iodine  will  readily  demonstrate  the  presence  of  such 
bacterial  films.  Under  favoring  circumstances  these  no  doubt  produce 
marginal  gum  irritation,  a  fact  proved  by  the  relief  of  such  a  con- 
dition by  the  mere  continued  cleansing  of  the  teeth — i.  e.,  the  removal 
of  the  plaques. 

Talbot^  has  demonstrated  that  a  deep  pocket  may  normally  exist 
at  the  gum  margin  favoring  the  retention  of  food  and  other  debris. 

Mechanical  causes  produce  direct  irritation;  these  are  deposits  of 
salivary  calculus  resting  upon  the  gum  or  beneath  the  gum  margin; 
fillings  projecting  beyond  cavity  margin ;  gum  overlying  cavity  margins; 
bruising  of  the  gum  margin  by  food  crowded  between  teeth  and 
removed  by  toothpicks;  the  fermentation  of  such  crowded  food;  the 
mechanical  action  of  toothpicks  or  floss  silk  improperly  crowded 
upon  the  gum  margin;  projecting  edges  of  artificial  crowns  or  bits 
of  cement  used  in  their  cementation;  tooth-brush  bristles;  fragments 
of  toothpicks,  bones,  or  oyster-shells,  etc. ;  rings  of  rubber  or  of  torn 
rubber  dam  or  ligatures  left  in  position;  improper  contact  of  the  edges 
of  prosthetic  plates  or  appliances  about  the  necks  of  teeth;  injuries 
inflicted  })y  rubber  dam  clamps,  wedges,  ligatures,  etc.;  the  eruption  of 
teeth  through  the  gums. 

The  action  of  any  of  these  causes  may  be  complicated  through  the 
infection  of  the  mechanically  irritated  part  by  oral  bacteria.     An 

•  Dental  Cosmos,  1894.  2  Ibid.,  1902.  "  Interstitial  Gingivitis. 


MARGINAL  GIXGIVITIS  593 

excellent  example  occurred  in  the  editor's  practice.  A  perfect  gum 
margin  was  irritated  by  the  margins  of  a  gutta-percha  cap  used  as  a 
remedy  for  hyperemia  of  the  pulp.  Pyogenic  organisms  produced  a 
marginal  suppuration  which  subsided  upon  removal  of  the  cap. 

Excessive  smoking  and  the  use  of  alcoholic  liquors  produce  local 
irritative  effects,  resulting  in  catarrhal  stomatitis  and  gingivitis. 

Lack  of  exercise  or  brushing  of  the  gums  produces  an  atonic  con- 
dition of  the  gum  margin,  predisposing  to  gingivitis  of  infective  char- 
acter. Too  persistent  brushing  with  stiff  brushes  may  be  equally 
injurious  by  causing  marginal  irritation. 

A  variety  of  marginal  gingivitis  exists  under  the  name  of  stomatitis 
ulcerosa;  the  cause  is  clearly  infective,  but  the  exact  bacterium  has  not 
yet  been  recognized.  It  tends  to  rapidly  penetrate  the  pericemental 
tissue.  The  gum  margin  has  a  pasty,  sloughing  appearance.  The 
ulceration  is  rapidly  cured  by  a  wash  consisting  of  mercuric  chloride 
in  hydrogen  dioxide  (1  to  2000). 

The  production  of  interstitial  gingivitis  by  causes  of  systemic  or 
drug  origin  involves  a  marginal  gingivitis,  but  marginal  gingivitis  is 
not  always  produced  by  local  causes  of  interstitial  gingivitis;  at  least, 
not  at  first. 

Pathology. — ^The  pathology  of  marginal  gingivitis  is  that  of  an 
inflammation  located  in  a  peculiar  situation — {.  e.,  in  the  marginal 
gum  tissue — and  tending  to  spread  into  the  deeper  interstitial  tissues. 
(See  Pathology  of  Interstitial  Gingivitis.) 

Symptoms. — ^The  symptoms  of  marginal  gingivitis  depend  upon  the 
cause.  When  mechanical  causes  are  acting  the  gum  presents  an 
inflamed  appearance;  it  is  swollen,' of  a  bright-red  or  purplish  color, 
very  sensitive  to  touch,  and  bleeds  readily. 

If  a  calculus  rest  against  the  gum,  the  latter  may  present  a  raw, 
chronically  inflamed  surface  in  contact  with  it.  A  ragged,  red,  split 
margin  of  gum  is  often  associated  with  calculus  upon  the  labial  surfaces 
of  lower  incisors,  cuspids,  and  bicuspids,  and  upper  cuspids  and 
bicuspids.  At  times  the  lingual  surfaces  of  the  lower  incisors  present 
such  an  appearance.  If  subgingival  calculus  be  present,  the  gum 
margin,  if  markedly  affected,  appears  loosened  and  is  of  a  flabby 
appearance  and  purplish  in  color.  In  some  cases  the  gum  margin 
appears  thickened  or  hypertrophied. 

A  bloodshot  appearance — i.  e.,  enlargement  of  terminal  vessels — is 
often  seen  in  gingivitis. 

In  cases  due  to  unhygienic  conditions — i.  e.,  food  collections  or 
38 


594     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

vitiated  secretions  about  the  necks  of  teeth — a  raw,  red,  outer  surface 
of  the  gum  margin  is  noted,  particularly  in  young  persons. 

In  stomatitis  ulcerosa  a  yellow,  pasty  ulceration  of  the  gum  margins 
may  occur.  It  is  rodent  in  character,  very  painful,  and  may  cause 
rapid  loss  of  the  pericementum  and  of  the  tooth.  In  gingivitis  due  to 
oral  infection  by  the  coccus  of  gonorrhea  an  intense  gingival  inflam- 
mation, with  looseness  of  the  teeth,  pyorrhea  alveolaris,  and  profuse 
salivation,  may  occur.^ 

Talbot^  describes  a  greenish  gray  glazed  surface  of  ulcerated 
raw  gum  in  two  cases  of  profuse  interstitial  gingivitis  due  to  the 
gonococcus. 

Cook  has  shown  that  stimulant  and  astringent  washes,  if  used  to 
excess,  have  a  degenerative  influence  upon  the  gum  margin.  (See  p. 
76.)     A  too  powerful  formaldehyde  wash  has  the  same  effect. 

Prognosis. — If  the  case  has  run  an  acute  course  and  is  due  to  the 
action  of  mechanical  causes  plus  infection,  recovery  is  usually  prompt 
upon  the  removal  of  the  cause  and  sterilization  of  the  injured  part. 
In  the  chronic  cases  due  to  the  more  slowly  acting  mechanical  and 
infective  causes  combined^ — e.  g.,  salivary  calculus  plus  infection — 
much  interstitial  gingivitis  may  have  occurred  accompanied  by  peri- 
cemental and  alveolar  resorption.  This  usually  constitutes  a  per- 
manent loss.  If  the  gum  margin  is  in  a  state  of  atony  or  inflammation 
as  the  result  of  collections  of  bacteria,  etc.,  upon  the  cervices  of  the 
teeth,  their  condition  may  be  improved  by  frequent  cleansings  of  the 
teeth. 

The  improvement  of  certain  chronic  malnutritional  disorders  may 
be  hoped  for  if  frequent  prophylaxis  be  practised  as  a  means  of  cause 
removal,  and  at  the  same  time  the  accumulated  waste  products  be 
eliminated  from  the  body  fluids  by  appropriate  means.  This  may, 
in  advanced  cases,  also  involve  the  treatment  of  diseased  organs. 

The  idea  of  systemic  infection  from  the  mouth  is  gaining  such 
headway  that  it  deserves  increased  prominence.  Even  should  its 
influence  be  overestimated,  it  will  serve  as  a  strong  argument  in  pre- 
senting the  subject  of  oral  prophylaxis  to  patients  who  unfortunately 
often  require  the  education  imparted  by  bitter  experience  in  order  to 
fully  grasp  its  importance. 

Treatment. — The  treatment  of  the  condition  consists  in  removing 
the  source  of  irritation  and  restoring  the  normal  circulation  in  the 

'  Vines,  British  Journiil  of  Dental  tsciences,  1903,  and  Dental  Cosnios,  1903. 
*  Dental  Cosmos,  1900. 


MARGINAL  GINGIVITIS  595 

parts.  If  the  source  of  the  disorder  be  in  some  underlying  constitu- 
tional condition,  the  symptoms  may  be  ameHorated,  although  not 
entirely  cured,  l)y  the  correction  of  the  general  disorder. 

Cases  due  to  mechanical  irritation  are  commonly  confined  to  one  or 
several  teeth,  rarely  to  an  entire  denture,  except  cases  continued  in  con- 
sequence of  deposits  of  scaly  calculi  beneath  the  gum  margin.  Foreign 
bodies,  such  as  bristles  and  fragments  of  bone,  should  ])e  removed. 
Projecting  fillings  or  overhanging  crown  margins  should  be  made 
flush  with  the  general  tooth  surface.  Salivary  calculi  should  be 
removed. 

Following  this,  perfect  cleansing  of  all  teeth  is  indicated,  this  to  be 
maintained  by  monthly  prophylaxis,  at  least,  until  the  case  is  cured. 

Antiseptic  mouth  washes  should  be  employed  frequently,  no  matter 
what  the  cause.  If  the  gum  tissue  be  soft  and  spongy,  showing  signs 
of  venous  hyperemia,  antiseptic  astringent  mouth  washes  should  be 
freely  used : 

I^. — Zinc,  chlorid gr.  x 

Aq.  menth.  pip. fgj — M. 

Increase  as  desired. 

The  above  preparation,  used  in  spray  from  an  atomizer  or  as  a 
wash  several  times  a  day,  is  an  excellent  local  application,  meeting 
both  indications.  Prescriptions  contahiing  eucalyptus  and  benzoic 
acid  are  excellent: 

I^. — Acid,  benzoic 3  parts 

Tinct.  eucalypti 15     " 

01.  menth.  pip 1  part 

Alcohol 100  parts 

Saccharin 2     "  — M. 

(Miller.) 

The  above  formula  diluted  one-half  is  agreeable  aiul  efficient. 
An  alkaline  1  per  cent,  salicylic  acid  wash  is  useful,  not  only  for 
the  gingivitis,  but  any  attendant  fetor  of  breath: 

I^. — Sodii  horatis 5iss 

Acidi  salicylic! gr.  xv 

Aquoe  mentha;  pip fSiij — Nf. 

The  following  is  astrhigent  and  antiseptic: 

I^. — Boroglycerini, 
Tinct.  krameriae, 
Tinct.  calenduloe, 

Alcoholis aa     fSJ — M. 

Sig. — One  or  two  teaspooufuls  to  a  small  glass  of  water. 


596      PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

Truman  advises  the  use  of  hydronaphthol  in  an  astringent  vehicle 
as  an  effective  germicide  for  use  by  a  patient : 

I^.— Hydronaphthol gr.  x 

Glycerol f3j 

Alcohol fg; 

Aquae  destil 15  J — M. 

Sig. — Use  as  a  wash  several  tunes  a  day.  (Peirce.) 

The  following  is  a  5  per  cent,  formaldehyde  solution  which,  diluted, 
can  be  used  as  a  mouth  wash,  having  astringent  and  antiseptic 
qualities.  It  is  also  useful  in  various  strengths  as  a  germicide  for 
root  canals.  A  formula  for  quantity  is  given,  which  may  be  reduced 
in  prescriptions: 

No.  1 

I^.— Thymol 3iss 

Menthol  5s3 

Oil  of  eucalyptus. 
Oil  of  gaultheria, 
Oil  of  cassia, 

Oil  of  cloves aa     f  3iss 

Alcohol fgij — M. 

No.  2 

Formaldehyde,  40  %  sol Oj 

Boric  acid. 

Sodium  biborate aa       5iij 

Water Oij— M. 

No.   3 
Water  to gal.  j. 

Make  up  No.  1  first,  and  shake  well.  Place  No.  2  in  a  gallon  demi- 
john, and  shake  well;  add  No.  1  and  shake  again;  add  No.  3  and  shake 
well.  For  dispensing  this  may  be  filtered;  for  ordinary  use  this  is 
not  necessary.  For  mouth  use  one-half  teaspoonful  is  to  be  diluted 
in  two  ounces  of  water,  making  a  1  to  600  formaldehyde  solution. 

Equal  parts  of  listerine  and  ordinary  distillate  of  hamamelis  is  a 
useful  combination.  Glycothymolin  is  a  very  popular  proprietary 
mouth  wash.     Phenol-sodique,  1  to  7  of  water,  is  quite  useful. 

For  mercurial  gingivitis  and  stomatitis,  the  following  has  been 
rationally  recommended  •} 

IJ. — Tinct.  myrrhae f  3iij 

Potassii  chloratis 3ss 

Sodii  chioridi 5ij 

Aquje  dist q.s.  ad  f^viij — M. 

Sig. — Use  as  mouth  wash.     Repeat  every  two  hours. 

All  mouth  washes  require  an  application  of  about  two  minutes' 
duration  at  least  twice  a  day  after  cleansing  the  teeth  in  order  to  pro- 

•  Medical  Press,  via  Dental  Cosmos. 


INTERSTITIAL  GINGIVITIS  597 

cluce  the  best  effects.  As  this  is  somewhat  fatiguing  to  the  oral 
muscles,  several  applications  may  be  made,  one  after  the  other, 
until  the  total  is  attained. 

For  the  restoration  of  gum  tissue  between  molars  and  bicuspids 
L.  Ashley  Faught^  has  recommended  a  few  applications  of  10  per 
cent,  trichloracetic  acid  on  an  orange-wood  stick  every  day  or  two 
until  the  case  is  cured. 

INTERSTITIAL  GINGIVITIS. 

Definition.^ — Interstitial  gingivitis  may  be  defined  as  an  inflammation 
characterized  by  the  presence  in  the  connective-tissue  elements  of  the 
pericementum  and  gum  tissue  of  an  excessive  number  of  leukocytes, 
attracted  thither  by  a  general  or  local  irritation  of  the  tissue  men- 
tioned. 

Causes. — ^Any  of  the  local  causes  producing  marginal  gingivitis,  if 
acting  deeply,  may  produce  a  general  or  interstitial  gingivitis.  In 
addition  to  these,  the  eruption  of  teeth,  the  wedging  of  them,  or  their 
movement  in  orthodontia,  in  short,  any  of  the  causes  of  pericementitis, 
septic  or  non-septic,  if  producing  inflammation  extending  beyond 
the  confines  of  the  pericementum,  necrosis,  or  ulceration  following 
extraction,  drug  or  metal  poisoning,  or  auto-intoxication,  whether 
gastro-intestinal  or  by  leucomaines,  and  acute  infectious  diseases, 
are  systemic  causes, 

A  case  of  spontaneous  loss  of  all  but  one  of  the  upper  teeth,  with 
subsequent  complete  alveolar  atrophy  as  the  residt  of  trophic 
disturbance  from  peripheral  neuritis  in  a  tabetic  woman,  has  been 
reported  by  Gaucher  and  Dobrovici,'  the  diagnosis  being  confirmed 
by  trophic  disturbance  in  the  foot  followed  by  plantar  perforation. 

General  Causes. — It  seems,  therefore,  quite  certain  that  in  condi- 
tions of  general  faulty  metabolism  substances  are  generated  in  the 
system  or  are  retained  by  reason  of  faulty  elimination,  and  which, 
floating  about  in  the  blood  stream,  act  as  irritants  to  the  pericementi 
and  gum  margins  about  the  teeth. 

Moreover,  the  pericemental  glands  seem  to  be  eliminating  organs 
which  may  become  overstimulated  and  thus  diseased. 

In  all  general  nutritional  disorders  parts  peripheral  to  the  circulation 
are  most  aft'ected,  become  debilitated,  and  tend  to  a  degenerative 
metamorphosis  of  cells. 

>  Dental  Cosmos,  1905.  '  Ibid.,  p.    1.505. 


598     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

Rhein  found  after  repeated  examinations  of  hospital  patients  that 
"marginal  gingivitis  was  an  accompaniment  of  typhoid  fever,  tuber- 
culosis, malarial  disorders,  acute  rheumatism,  pleurisy,  pericarditis, 
and  S}'philis,  among  the  acute  diseases.  Of  chronic  nutritional  diseases, 
it  was  commonly  observed  in  cases  of  gout,  diabetes,  chronic  rheuma- 
tism, several  forms  of  nephritis,  scurvy,  chlorosis,  anemia,  leukemia, 
and  pregnancy.  Also  in  disorders  of  the  central  nervous  system  and 
following  the  administration  of  mercury,  lead,  and  iodine." 

Rhem  states  that  the  gingivitis  produced  by  any  of  these  diseases 
has  distinctive  features  which  may  even  serve  as  diagnostic  signs  of 
the  nature  of  the  general  malady. 

Talbot's  experiments  in  the  mercurialization  of  dogs  (see  Interstitial 
Gingivitis)  demonstrate  that  efforts  upon  the  part  of  the  perice- 
mentum to  eliminate  the  bichloride  of  mercury  result  in  a  non-septic 
pericementitis,  exhibiting  in  its  morbid  anatomy  the  characteristic 
round-celled  infiltration  of  inflammation. 

Black^  has  shown  that  a  gingivitis  produced  by  the  systemic  admin- 
istration of  potassium  iodide  may  be  proved  to  be  caused  by  its  elimi- 
nation by  the  pericemental  glands  by  test  of  the  gingival  secretion  for 
the  iodine  reaction. 

It  is  quite  reasonable  to  suppose  that  irritative  substances  originating 
in  the  body  and  floating  in  the  blood  stream  may  act  in  like  manner. 
This  has  been  termed  auto-intoxication. 

Irritation  resulting  from  the  administration  of  mercury,  lead,  and 
iodine,  or  from  toxic  substances  absorbed  from  the  intestines,  is,  of 
course,  extrinsic  intoxication. 

It  has  been  claimed  by  Hunter,  Herschell,  Goadby,  W.  B.  Keyes, 
D,  D.  Smith,  and  others,  that  the  toxins  formed  by  oral  fermenta- 
tions and  the  septic  infection  of  the  stomach,  intestines,  etc.,  arising 
from  the  mouth  are  competent  to  excite  a  train  of  systemic  disturb- 
ances ending  in  a  general  malnutrition. 

Certain  accomplished  cures  of  such  states  by  constant  oral  prophy- 
laxis lend  plausibility  if  not  certain  proof  to  this  argument.  Still, 
the  malnutrition,  whatever  its  cause,  oral  or  otherwise,  may  become 
a  predisposition  l)y  lessening  the  resistance  of  the  soft  parts  about 
the  teeth. 

Talbot  claims  that  interstitial  gingivitis  is  largely  due  to  auto- 
intoxication due  to  intestinal  fermentation  witli  production  of  by- 
products, notal)ly  indol,  which,  when  absorbed,  may  or  may  not  be 

'  American  System  of  Dentistry. 


INTERSTITIAL  GINGIVITIS  599 

eliminated  through  the  ehminating  organs — liver,  kidneys,  skin,  and 
lungs — and  that  if  these  be  insufficient  to  the  task,  retention 
occurs  and  even  further  disease  of  the  organs  themselves,  especially 
the  kidneys.  Constipation  aggravates  the  contlition  if  not  producing 
it  by  retention  of  fecal  matter,  with  which  the  poisons  should  be 
eliminated.  The  overstrain  of  the  kidney  in  the  endeavor  to  take  up 
the  work  of  the  liver  (when  that  is  diseased)  in  elimination,  produces 
renal  inflammation  and  impairment  of  eliminative  function. 

The  blood  is  surcharged  with  accumulated  poisons,  the  heart  and 
arteries  degenerate,  and  cardiac  hypertrophy  and  arteriosclerosis  are 
produced.  Blood  pressure  is  increased  and  end  artery  and  nerve 
degeneration  occur,  in  the  brain,  eye,  alveolar  process,  pulp,  etc., 
being  noticeable  first  in  the  gums.  He  draws  attention  to  the  transitory 
nature  of  the  alveolar  process,  and  the  inability  of  the  arteries  to 
expand,  as  in  soft  tissues,  and  that  poisonous  products  settle  in  the 
end  arteries,  and  points  out  that  gingivitis  is  a  natural  result  of  these 
conditions.  The  demonstration  of  infarction  in  the  pulp  due  to 
systemic  conditions,  even  in  the  young,  has  been  made  by  Hopewell- 
Smith    (see  p.  461),   and   also   indicates  end-artery  strain. 

Talbot  regards  indican,  the  product  of  indol,  which  is  found  in  the 
urine,  as  the  excitant  of  ghigivitis  in  intestinal  fermentation  (auto- 
intoxication), and  the  general  acidosis,  as  indicated  either  by  an  excess 
of  acidity  in  the  urine  or  a  deficiency  therein,  as  excitant  in  various 
conditions  of  malnutrition. 

The  excess  of  acidity  above  40°  in  the  urine  indicates  excessively 
imperfect  oxidation,  while  defective  acidity  (below  30°)  indicates 
insufficiency  of  renal  elimination.  In  both  cases  systemic  acidosis  is 
the  condition.     (See  p.  94.) 

Diagnosis  of  Systemic  Causes. — In  the  diagnosis  of  systemic 
cause  by  malnutritional  conditions  twenty-four-hour  urine  should  be 
obtained  and  the  following  points  looked  for.^  (See  also  pages  87 
and  28C.) 

Amount. — This  should  be  about  forty  ounces. 

Specific  Gravity. — If  high,  it  indicates  an  increased  proportion  of 
solids  ])or  ounce. 

Degree  of  Acidity. — If  above  40°  it  indicates  acidosis  by  imperfect 
oxidation;  if  below  30°  it  indicates  renal  insufficiency  and  retention 
in  blood  of  acid  proilucts. 

>  Talbot,  Interstitial  Gingivitis  due  to  Auto-intoxipation.  .Tonrnal  Amorioan  Arodical  Asso- 
ciation anil  Dental  Digest,  190G. 


600     PERICEMENTAL  DISEASES  BEGINNING  AT    GUM  MARGIN 


Indican. — If  present,  it  always  indicates  intestinal  fermentation,  and 
cases  of  interstitial  gingivitis  have  it  with  production  of  indol. 

Albumin, — Not  of  certain  origin. 

Hyaline  Casts. — If  bloody,  they  indicate  renal  inflammation. 

Compound  Hyaline  and  Coarsely  Granular  Casts  and  Waxy  and  Amyloid 
Casts. — Indicate  changes  in  structure  of  kidney. 

Symptoms. — Headache,  loss  of  appetite,  loss  of  memory,  irritability, 
biliousness,  fatigue,  muscle  soreness,  hypochondriasis,  insomnia,  ver- 
tigo, muddy  complexion,  tinnitus  aurium,  general  nervousness,  cold 
extremities,  impotence,  leg  cramps,  twitching  of  muscles,  neurasthenia, 
pruritis,  acne,  urticaria,  arteriosclerosis,  gout,  rheumatism,  Bright's 
disease,  diabetes,  uric  acid  diathesis,  nervous  disorders,  asthma, 
anemia,  lethargy,  stupor,  insanity,  etc.,  are  symptoms  which,  in  part, 
may  develop  from  the  auto-intoxication  by  the  toxins  and  acidosis. 
(See  General  Malnutrition.) 

Unnatural  odor  of   the   breath,  armpits,  and  thighs  indicate   an 


effort  of  the  lungs  and  skin  at  elimination.^ 


Fig.  478 


Fig.  479 


Fig.  480 


Resorption  of  alveolar   process   clue    to   interstitial   gingivitis,  caused   by  marginal   irritation 
from  excessive  filling  material.     (Radiographs  by  Price.) 

Pathology  and  Morbid  Anatomy. — The  local  or  systemic  causes 
produce  direct  inflammation;  waste  products  collected  in  the  end 
arteries  produce  local  degeneration,  and  the  bloodvessels  become  over- 
full, diapedesis  of  leukocytes  into  the  interstitial  submucous  gum 
tissue  occurs,  and  the  spaces  are  filled  with  inflammatory  exudate. 
The  papillae  become  enlarged  and  the  epithelial  layer  undergoes  an 
increa.se  in  formation  of  cells  (hyperplasia).  The  gum  in  consequence 
of  these  changes  becomes  swollen,  its  color  deepened,  and  it  bleeds 
readily. 

If  the  process  be  advanced  the  alveolar  process  is  involved. 

After  a  time  the  effects  of  continued  low-grade  inflammation  are 
expressed  in  resorption  of  bone  or  cementum,  or  both,  or  hypertrophy 


'  Talbot. 


INTERSTITIAL  GINGIVITIS  001 

of  bone  or  cementum,  or  both,  or  the  two  processes  may  be  in  evidence 
at  the  same  time. 

If  at  any  time  pyogenic  infection  occur  at  the  gum  margin,  the 
purulent  phenomenon  of  pyorrhea  alveolaris  is  produced. 

Following  resorption  of  the  alveolar  process  the  teeth  loosen,  more 
irritation  occurs,  infection  has  a  deeper  action,  calculi  may  form  on 
the  roots,  and  the  teeth  are  finally  lost.  Talbot  describes  several 
forms  of  bone  resorption  occurring  in  interstitial  gingivitis : 

(a)  Lacunar  resorption  carried  on  by  the  osteoclasts  normally  lying 
upon  the  surface  of  the  bone.  Under  irritation  they  increase  in  number 
and  excavate  irregular  bays  in  the  bone  (Howship's  lacunge).  These  are 
then  deepened  and  widened,  destroying  areas  of  bone.     (See  Fig.  73.) 

(6)  Perforating  canal  resorption  beginning  in  the  small  canals 
normally  perforating  the  trabecular  of  bone  in  various  directions  and 
transmitting  the  bloodvessels  from  one  medullary  space  or  Haversian 
canal  to  another  (Volkmann's  canals).  The  osteoclasts  widen  these, 
necessarily  reducing  the  substance  of  the  trabeculse  (Fig.  71). 

(c)  Halisteresis  ossium,  beginning  with  a  decalcification  of  masses  of 
the  bone,  the  organic  matrix  being  for  a  time  undisturbed,  but  is  later 
removed.  This  is  a  local  expression  of  what  may  occur  in  other  bones 
of  the  body  in  the  condition  known  as  osteomalacia  (Fig.  74.) 

According  to  Talbot  premature  resorption  of  the  alveolar  margins, 
either  local  or  general,  is  due  to  this  process,  called  by  him  alveolar 
osteomalacia,  and  occurs  in  pregnancy  or  senility,  as  a  rule. 

He  states  that  the  decalcified  bones  may  be  recalcified  after  confine- 
ment in  pregnancy,  but  is  never  restored  in  senility. 

A  lesser  degree  of  irritation  may  set  the  osteoblasts  at  work  and 
cause  the  building  up  of  the  alveolar  process,  either  as  a  restoration  of 
resorbed  bone  or  as  an  hypertrophy  of  either  the  alveolar  process  or 
the  cementum  of  the  root  (liypercementosis). 

Endarteritis  obliterans  is  a  thickening;  of  the  intima  of  an  arterv 
or  capillary,  due  to  chronic  irritation,  and  causing  a  lessening  of  the 
lumen  of  the  vessel,  even  to  the  poiht  of  obliteration  of  the  capillaries. 

The  blood  flow  is  impeded  and  nutrition  of  cells  impaired.  Any 
cause  of  interstitial  inflammation  may  produce  it.  In  all  cases  of 
chronic  interstitial  gingivitis  the  bloodvessels  are  so  diseased  (Figs. 
481  and  482). 

Local  Treatment. — The  treatment  must  be  directed  to  the  removal 
of  the  underlying  cause,  whether  local  or  systemic.  In  adtlition,  if 
a  general  gingivitis  be  present  or  a  local  gingivitis  amenable  to  external 


602     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM   MARGIN 

treatment,  the  application  of  iodoglycerol,  together  with  fixation  of 
the  teeth  if  needed  and  possible,  is  indicated  (Talbot^). 

I^. — Zinc  iodide 15  grams. 

Iodine 25      " 

Glycerin 50      " 

Water 10      "  — M. 

Apply  on  cotton  wound  on  an  orange-wood  stick  or  metal  applicator, 
freely  to  all  gum  surfaces,  and  dry  each  after  painting.  If  teeth  are 
hopeless  they  should  be  extracted,  otherwise  they  maintain  the 
condition. 


Fig.  481 


Fig.  482 


Longitudinal  sectinri  ol  gingiv^al  border,  showing  round- 
cell  inflammation,  due  to  mercury,  and  extending  to  the 
inner  coat  of  the  bloodvessel,  and  also  plasma  mast  cells. 
From  a  dog.     (Talbot.) 


Endarteritis  obliterans:  A, 
adventitia;  E,  elastic  tissue 
between  middle  coat  and  in- 
tima;  M,  muscular  coat;  J, 
thickened  intima.  (Talbot, 
after  Kaufmann.) 


Systemic  Treatment. — The  restoration  of  the  eliminative  function 
should  ])e  aimed  at.  In  intestinal  auto-intoxication  impacted  fecal 
matter  should  be  removed  by  repeated  injections,  if  necessary,  of  warm 
water,  and  the  bowels  be  kept  clear  by  flushing  with  soap  and  water 
once  or  twice  a  week.  The  massage  of  the  abdomen  restores  the 
tonicity  of  the  bowels.  The  bile  function  should  be  restored,  and 
the  bile  l)e  increased  in  flow  by  calomel  and  soda,  ty  to  ^  gr., 
every  hour  until  1  grain  is  taken;  to  be  followed  by  a  saline  laxative 
(as  Seidlitz  powder);  or  podophyllin,  yV  to  ^  gr.,  up  to  \  gr.,  may  be 
given  instead  of  calomel. 


'  Dental  Cosmos.  1905.  p.  1.312. 


MARGINAL  ATROPHY  OF  THE  GUMS  003 

Talbot*  also  uses: 

I^. — Aldiu ?    e^"- 

Strycliiiine  sulpliate 7/,;    gr. 

Extract  belladonna s"     gr. 

Pulv.  Ipecac j\    gr. — M. 

Take  at  bedtime  and  follow  with  a  saline  cathartic  next  morning. 
If  the  stools  remain  unhealthy,  administer  each  two  to  four  hours  2 
to  5  gr.  of  compound  lime,  soda  and  zinc  carbolate  until  the  stools 
are  healthy. 

To  continue  the  stimulation  of  the  liver  administer  bilein  iV  to  ^  gr. 
four  or  five  times  a  day. 

The  urine  should  be  examined  for  evidence  of  established  disease, 
and  if  this  be  found  the  patient  referred  to  a  general  practitioner.  (See 
General  Malnutrition.)  If  found  only  symptomatic  of  hepatic  or 
renal  insufficiency  and  nutritional  disorder,  the  amount  should  be 
increased  to  40  ounces  by  the  drinking  of  3  pints  of  water  (including 
table  beverages)  per  day,  which  will  aid  bowel  and  renal  elimination 
and  flush  tissues  of  accumulations,  including  retained  acids.  If  the 
urine  be  abnormally  acid  (above  40°)  administer  3-gr.  tablet  of  lithia, 
sodium  bicarbonate,  or  sodium  chloride  in  a  glass  of  water  four  times 
a  day.  Hot  or  Turkish  baths  keep  the  skin  free  for  eliminative 
finiction.  Well-apportioned  rest  and  exercise  and  moderate  eating 
of  proper  nutritious  food  are  indicated.     (See  pages  88  and  97.) 


MARGINAL  ATROPHY  OF  THE  GUMS. 

In  advanced  age  there  exists  often  a  tendency  of  the  gums  to  shrink 
evenly  away  from  the  enamel,  exposing  the  cementum.  Hopewell- 
Smith  describes  this  as  accompanied  by  fibroid  degeneration  of 
the  pericementum,  and  regards  the  latter  as  a  purely  senile  change. 

It  may  be  noted  upon  the  buccal  side  only  of  a  denture,  and  be  due 
to  vigorous  brushing. 

It  is  also  seen  localized  at  cervices  next  to  a  space  from  which  a 
tooth  has  been  extracted.  In  one  case  the  editor  saw  a  slightly 
hypertrophied  gum  distinctly  overlapping  a  cavity  margin  drawn 
back  one-eighth  inch  within  a  month  as  the  result  of  exkfaction  of  the 
adjoining  root. 

'  Tlierapeutics  and  Treatment  of  Interstitial  Gingivitis,  Dental  Digest,  190G. 


604     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

Apart  from  senile  changes,  and  possibly  even  including  them,  these 
effects  seem  to  be  the  result  of  an  overstimulation  of  the  gums  resulting 
in  atrophy.  It  may  be  that  collections  upon  the  teeth  are  in  some 
degree  responsible.  The  gums  have,  for  the  most  part,  a  healthy  look, 
but  are  in  a  condition  predisposed  to  pyorrhea  alveolaris. 

Treatment. — If  localized  and  the  restoration  of  the  gum  be  desirable, 
Harlan's  method  may  be  tried. ^  (1)  Cleanse  the  exposed  tooth 
surface  and  slightly  roughen  it  near  the  gum  margin.  (2)  Dissect 
away  the  gum  from  the  root  to  about  one-quarter  inch  in  depth, 
wiping  the  blood  away  carefully  with  mouth  open  until  hemorrhage 

Fig.  483 


Recession  of  gum  in  senility;   beginning  decalcification  of  cementum;  alveolar  resorption 
after  extraction.     (Philadelphia  Dental  College  Museum.) 

ceases  spontaneously,  or  check  with  adrenalin  solution,  (3)  Make 
three  incisions  into  and  through  the  gum  tissue.  (4)  Wlien  bleeding 
has  almost  ceased  fill  the  cuts  with  dried  zinc  iodide,  allowing  the 
blood  to  liquefy  it  so  that  it  may  be  carried  around  the  gum  margin. 
This  creates  a  profound  irritation,  which  should  not  be  disturbed. 
(5)  The  patient  should  use  a  mild  antacid  antiseptic  wash,  as  of 
sodium  bicarbonate  or  milk  of  magnesia.  (6)  Repeat  three  or  four 
times  at  intervals  of  three  or  four  weeks,  with  cuts  in  a  new  location. 
(7)  Use  silk  or  pure  silver  ligatures  around  the  teeth  under  the 
gum    for  further  irritation.      (8)  To  allay  overirritation  paint  with 

1  Dental  Cosmo.s,  1906,  p.  927,  and  1907,  p.  598. 


MARGINAL  ATROPHY  OF  THE  GUMS  6U5 

1  part  adrenalin  and  3  parts  compound  tincture  of  iodine  once  in 
three  days. 

Harlan  states  that  a  long  time  may  be  required  in  some  cases.  It 
should  not  be  attempted  over  a  gold  filling,  but  an  unglazed  porcelain 
may  be  covered,  though  no  attachment  will  exist.  The  principle  in- 
volved is  that  of  coaxing  the  gum  into  adherence  with  the  roughened 
root,  and  the  filling  in  of  the  cut  with  scar  tissue. 

As  a  wash  use : 

I^. — Hydronaplitliol gr    xx  , 

Oil  eucalyptus    ....  TH  x 

Oil  ca.ssia      ....  IH  x 

Alcohol fo'ij 

Distilled  water fSxiij — M. 

Sig. — Use  freely  five  or  six  times  daily,  diluted,  if  neces.-^ry,  with   more  water. 

The  gums  should  not  be  brushed  for  several  days  after  operating. 
Avoid  insoluble  dentifrices. 

For  general  recession  due  to  osteomalacia  the  general  acidosis  may 
be  treated. 


CHAPTERXXIII. 
SALIVARY  AND  SERUMAL  CALCULUS. 

Calculi  are  more  or  less  hard  concretions  found  in  varying  situa- 
tions and  composed  of  inorganic  and  organic  matter  combined  in  an 
unknown  manner. 

As  related  to  the  teeth,  calculi  arise  from  the  following  recognized 
sources : 

1.  Obviously  from  the  saliva,  and  deposited  in  situations  which 
clearly  indicate  its  source,  salivary  calculus  (or  ptyalogenic  calculus — 
Peirce). 

2.  From  the  serum  of  the  blood  deposited  at  some  point  along  the 
side  of  the  root  between  the  gum  margin  and  the  apex  of  the  root,  and 
called  serumal  calculus  (Black),  or  sanguinary  calculus  (Ingersoll). 
Of  this  there  are  several  varieties : 

(a)  That  associated  with  a  probable  fermentation  and  an  altered 
secretion  from  the  gum  margin,  and  known  as  subgingival  calculus. 

(b)  That  occurring  in  situations  in  which  a  chronic  pus  flow  is 
found,  whether  apical  or  subgingival,  and  which  may  be  called 
pyogenic  calculus. 

(c)  That  found  upon  the  roots  of  teeth  at  a  point  to  which  saliva 
has  no  access  and  over  which  pus  does  not  flow,  and  which  is  therefore 
deposited  by  the  lymph  derived  from  the  blood,  and  to  which  the 
appellation  hematogenic  calculus  (Peirce)  is  applicable. 

In  this  class  Kirk  found  two  varieties  resulting  from  pericemental 
inflammation:  (1)  subpericemental  deposits,  and  (2)  intrapericemental 
deposits.^ 

These  several  names  will  be  adhered  to  in  further  descriptions  as 
having  definite  significance. 

SALIVARY  CALCULUS. 

Definition. — Salivary  or  ptyalogenic  calculi  are  hard  formations 
composed  of  salts  of  the  saliva  which  have  been  deposited  or  pre- 

'  Dental  Cosmos,  1905. 


SALTVARY  CALCULUS 


607 


cipitated  and  combined  in  an  unknown  manner  with  organic  sub- 
stances, probably  mucin  or  gl<)l)ulin. 

Occurrence. — They  are  found  upon  the  surfaces  of  the  teeth, 
notably  in  situations  opposite  the  mouths  of  the  salivary  glands,  in 
the  ducts  of  the  muciparous  salivary  glands  (sublingual  and  sub- 
maxillary), and  upon  artificial  dentures.  A  photograph  of  a  plate' 
containing  an  enormous  mass  of  calculus,  the  result  of  seven  years' 
accumulation,  is  shown  in  Fig.  484.  The  teeth  are  occasionally 
buried  in  it.  The  editor  extracted  three  lower  incisors  which  had 
been  wired  together,  and  were  absolutely  covered  from  the  neck  to 
the  apex  by  calculus. 

Varieties. — Clinically  two  distinct  varieties  of  salivary  calculus  are 
recognizable:  (1)  the  soft,  friable,  whitish  yellow  deposits  found 
chiefly  upon  the  buccal  surfaces 

of  the   upper   molars   and    upon  ^'°-  ^^^ 

tlie  lingual  surfaces  of  the  lower 
anterior  teeth;  (2)  dark-colored 
and  hard  deposits  found  more 
frequently  in  the  latter  situation, 
less  frequently  in  the  former. 

Origin  of  Salivary  Calculus. — 
The  origin  of  salivary  calculus 
may  be  studied  from  several 
standpoints:  (1)  the  formation 
of  calculi  in  other  parts  of  the 
body;  (2)  an  analysis  of  saliva 
and  salivary  calculi;  (3)  extra- 
oral  experiments  upon  saliva  with 
a  view  to  the  formation  of  salivary 

calculus  extra-orally;  (4)    the   changes   observed    clinically  in    sali- 
vary calculus  during  its  deposition. 

Ziegler^  states  that  all  free  concretions  have  an  organic  basis  or 
nucleus  (inspissated  feces,  vegetable  material,  epithelial  scales, 
mucus,  etc.). 

As  to  cholesterui  gallstones,  he  states  that  if  the  cholesterin  be 
dissolved  out  by  ether,  a  yellowish  organic  matrix  remains  which 
retains  the  form  of  the  stone  and  presents  upon  examination  radiating 
spaces  formerly  occupied  by  the  crystals.  lie  describes  the  formation 
of  the  gallstone  as  an  infiltration  or  incrustation  of  deirenerated  oruanic 


Salivary  calculus  attached  to  a  lower  partial 
plate  worn  seven  years  without  removal. 
Shows  form  of  sublingual  space.  Practice  of 
Dr.  Ford,  Toulouse,  France.  (Siiecimen  in 
possession  of  Philadelphia  Academy  of 
Stomatology.) 


1  Possession  of  Academy  of  Stomatology  of  Philadelphia. 


^  General  Pathology. 


608  SALIVARY  AXD  SERUMAL  CALCULUS 

matter  (epithelial  scales,  etc.)  with  cholesterin,  bile  pigment,  etc.,  to 
which,  after  a  nucleus  is  formed,  other  portions  are  added  in  like 
manner. 

Of  urmary  calculi  he  states  that  Ebstein  has  shown  an  organic 
substance  albuminous  in  nature  to  be  left  after  dissolving  out  the 
various  salts. 

In  stratified  calculi  this  stroma  also  shows  stratification.  Such  a 
stroma  may  be  seen  after  decalcification  of  a  bit  of  salivary  calculus. 

Analysis  of  salivary  calculus  shows  it  to  be  composed  of  about  22  per 
cent,  of  water  and  organic  matter  as  the  portion  removable  by  burning 
the  calculus,  and  about  78  per  cent,  inorganic  matter  as  the  portion 
removable  by  decalcification  with  acids. 

Following  are  the  analyses  of  salivary  calculus  by  Stevenson  and 
Schehevetskey,  respectively  •} 

Soft  tartar  Hard  tartar  on 

on  molars.  lower  incisors. 

Water  and  organic  matter 21.48  17.51 

Magnesium  phosphate 1.31  1.31 

Calcimn   phosphate  with   a   little    carbonate   and 

trace  of  fluoride 77.21  81.18 

100.00  100.00 

Water  and  organic  matter 22.07 

Magnesium  phosphate 1-07 

Calcium  phosphate 67.18 

Calcium  carbonate 8.13 

Calcium  fluoride 1.55 

100.00 

These  observers  are  practically  agreed  upon  the  substances  present 
in  calculus  as  mainly  calcium  phosphate  with  some  calcium  carbonate, 
calcium  fluoride,  and  magnesium  phosphate  combined  with  organic 
matter. 

Talbot  furnishes  the  following  analysis  of  serumal  calculus  by 
J.  H.  Salisbury:^ 

Water  and  organic  matter 32.24 

Magnesium  phosphate 0.98 

Calcium  phosphate 63.08 

Calcium  carbonate 3  70 

100.00 

To  these  Kirk^  adds  ammoniomagnesium  phosphate  as  a  product 
of  putrefaction. 

»  Talbot,   Interstitial    Gingivitis.  *  Ibid. 

3  Dental  Cosmos.  1905,  p.  752. 


SALIVARY   CALCULUS  609 

According  to  Mitscherlich/  parotid  saliva  contains  globulin,  hut  no 
mucin,  and  contains  calcium  carbonate;  calcium  j^hospliate  l)eing 
present  in  but  minute  amount.  The  submaxillary  saliva  contains  a 
large  amount  of  mucin,  whicli  gives  to  mixed  saliva  its  viscid  nature. 

Analyses  of  submaxillary  saliva  and  mixed  saliva  by  Bitlder  and 
Schmidt  gave  the  following  results : 

Submaxillary  Saliva. 

Water 991.45 

Organic  matter 2.89 

f  Calrium  chloride             ^  a  -n 

I  Sodium  chloride  J 

Inorganic  matter  -i   ,,  ,   .  ,         ,  ^ 

I  (  ak'ium  carljonate         | 

I  ("alcium  phospliate         !- 1.16 

L  Magnesium  phosphate  J  

1000.00 

Mixed  Saliva. 

Water 995.16 

^         .  (  Epithelium 1.62 

Organic    niatter    ^,  ^ji    ui               •          *.  ^  ia 

(  Soluble  orgamc  matter 1.34 

r  Potas.sium  .sulphocyanide       .  0.06 

Inorganic  matter  <  Sodium,  calcium,  and  magnesium  pho.sphate        .  0.98 

I.  Sodium  and  potassium  chloride 0.84 

1000.00 

That  an  error  of  experiment  or  estimation  exists  in  these  analyses 
is  shown  by  the  fact  that  calcium  carbonate  is  not  mentioned  as 
existing  in  mixed  saliva,  while  it  exists  in  submaxillary  saliva;  this  is 
a  physical  impossibility. 

It  is  presumptive,  however,  that  calcium  carbonate  has  not  been 
specially  estimated. 

The  blood  contains  about  0.8  per  cent,  of  inorganic  salts,  including 
those  found  in  salivary  calculi,  and  a  certain  percentage  of  them  is  also 
found  in  the  blood  corpuscles.  They  probably,  therefore,  exist  in 
body  cells  in  some  proportion. 

The  salts  are  also  taken  into  the  body  in  the  form  of  food.  Their 
appearance  in  the  various  excretions  and  secretions  of  the  body  is  to 
be  regarded  as  in  all  probability  an  effort  upon  the  part  of  the  system 
to  eliminate  a  superabundance  of  inorganic  material  from  the  body. 

The  ingestion  of  quantities  of  animal  or  vegetable  foo<l  rich  in 
phosphates,  or  the  excessive  liberation  of  the  phosphoric  acid  in  mal- 
nutrition, may  produce  an  excessive  elimination  of  these  in  the  excre- 
tions and  cause  a  tendency  to  the  production  of  calculi  about  the  body. 

'  Halliburton,  Physiological  and  Pathological  Chemistry. 

3'J 


610  SALIVARY  AND  SERUMAL  CALCULUS 

This  condition,  known  as  phosphaturia,  is  observed  in  certain  nervous 
diseases,  rachitis,  osteomalacia,  leukemia,  gout,  and  rheumatism,^  in 
which  the  phosphaturia  is  symptomatic  of  an  excessive  katabolism; 
also  in  intestinal  disturbance  resulting  in  imperfect  assimilation  of 
food.     (See  p.  88.) 

^Miether  taken  in  as  food  or  liberated  during  metabolism,  it  is 
probable,  as  pointed  out  by  Talbot,  that  if  one  excretory  organ  fail  to 
perform  its  office  in  full  degree  another  must  take  up  its  work.  For 
this  reason,  in  any  bodily  condition  aifecting  elimination  a  super- 
abundance of  inorganic  salts  may  appear  in  the  blood  and  hence 
in  the  saliva,  and,  probably,  in  even  the  secretions  from  the  gingival 
margins. 

That  the  deposit  of  calculus  is  mainly  dependent  upon  the  super- 
abundance of  calcium  salts  in  the  saliva  is  evidenced  by  the  fact  that 
in  young  children  but  little  calculus  is  deposited  upon  the  teeth, 
though  the  oral  fermentation  is  not  lacking. 

If  a  bit  of  calculus  be  dried  and  then  burned  at  a  red  heat,  the  organic 
matter  present  will  burn  out,  the  calculus  retaining  its  form.     If  a 

similar  bit  be  subjected   to  a  di- 
^'"•^^^  lute  acid  (1  per  cent,  nitric),  the 

inorganic  matter  will  be  removed, 
the  calculus  will  float  to  the  top 
/^'^:  of  the  liquid,  and,  after   a  time, 

remain  as  a  light  stroma  of 
nearly  the  original  form  of  the 
piece. 

If  a  bit  of  calculus  be  trans- 

A,  nidus;  B,  calculus.  i  i     -j    •  i 

versely  ground,  it  is  seen  under  a 
low-power  lens  to  present  a  laminated  appearance — i.  e.,  it  has  been 
deposited  in  layers  representing  periods  of  activity.  The  under 
surface  of  the  calculus  shows  a  concentric  formation.  Beneath  the 
mass  a  nidus  of  darker  calculus  may  be  found,  and  if  section  of  exten- 
sive calculi  be  made  the  greenish  deposits  may  be  seen  scattered 
through  the  mass.  Black  has  noted  the  presence  of  urates  in  nearly 
all  specimens  examined  by  the  murexide  test.  Foreign  bodies  are 
sometimes  entangled  in  the  mass.  Peirce  recorded  a  case  in  which 
a  small  clasp  plate  was  securely  fastened  to  the  teeth,  and  the  patient 
denied  possession  of  such  a  substitute. 

In  some  cases  extensive  salivary  deposits  are  found  associated  with 

'  Thompson,  Practical  Medicine. 


SALIVARY  CALCULUS  GU 

highly  offensive  odors — i.  e.,  putrefaction  of  the  organic  matter  occurs 
as  a  part  of  the  process — indeed,  bacteria  are  constantly  associated 
with  the  mass  and  may  furnish  their  quota  of  the  organic  matter. 
Extraneous  matters,  such  as  tobacco-smoke  or  other  pigments,  cause 
discoloration  of  the  mass.  \Mth  data  relative  to  the  physical  and 
chemical  analysis  of  calculi,  the  mode  of  calcidus  formation  may  be 
studied.  It  will  be  noted  that  the  necessary  elements  of  calculus 
formation  are  supplied  by  the  saliva  and  food  debris — i.  e.,  an 
organic  basis  is  furnished  in  which  calcium  salts  may  be  entangled, 
precipitated,  or  chemically  combined. 

Mode  of  Calculus  Formation. — If  a  test-tube  be  filled  with  saliva  and 
allowed  to  remain  at  rest  for  several  days,  a  flocculent,  light  yellow 
precipitate  will  be  noted  at  the  bottom  of  the  tube.  If  the  supernatant 
fluid  be  drawn  off  with  a  pipette  and  the  precipitate  be  allowed  to 
dry,  it  will  be  found  possessed  of  the  chief  characteristics  of  calculus — 
hardness,  friability,  a  light  yellow  color,  tenacity  of  adherence  to 
objects  with  which  it  is  in  contact,  and  capability  of  analysis  into 
organic  matter  and  inorganic  salts. 

Various  theories  are  held  as  to  the  mode  of  precipitation  of  the 
calculus  upon  the  teeth,  the  most  plausible  and  capable  of  demon- 
stration being  that  the  calcium  salts  are  held  in  loose  suspension  by 
carbon  dioxide  in  the  body  fluid.  As  the  carbon  dioxide  escapes 
the  calcium  salts  precipitate,  but  become  combined  with  a  certain 
percentage  of  the  albuminous  elements  of  the  saliva — i.  e.,  globulin 
and  mucin.  As  this  will  occur  in  saliva  with  alkaline  reaction,  and 
even  in  that  undergoing  putrefaction,  it  is  not  likely  that  an  acid 
reaction  of  the  saliva  has  much  to  do  with  deposition  of  calcidus; 
neither  is  it  likely  that  the  carbon  dioxide  of  the  breath  causes 
deposition  of  the  calcium  as  claimed,  as  calcium  phosphate  is  the 
chief  salt  in  calculus  rather  than  calcium  carbonate.  The  latter  idea 
also  fails  to  accoiuit  for  serumal  calculus.  At  the  same  time  the 
abnormal  local  acidity  of  degenerative  tissue  is  considered  to  favor 
deposition  of  hematogenic  calculus.     (See  p.  94.) 

Exposure  of  the  roots  of  teeth,  especially  the  lower  anterior  ones, 
favors  the  deposition  of  calculus  owing  to  the  difficulty  of  brushing 
the  surfaces. 

That  rest  or  relative  quiescence  of  the  saliva  is  necessary  for  the 
formation  of  calcidus  is  shown  by  the  fact  that  it  occurs  at  points 
which  are  ordinarily  not  subjected  to  agitation — ?.  c,  buccal  surfaces 
of  upper  molars,  lingual  and  labial  surfaces  of  lower  incisors. 


612 


SALIVARY  AND  SERUMAL  CALCULUS 


Adhesive  precipitations  of  newly  formed  and  very  soft  calculus  form 
in  these  latter  situations  in  the  course  of  twenty-four  hours.  If  not 
removed  by  brushing  they  harden  and  thicken.     An  unused  side  of 


Fig.  486 


Fig.  487 


Unclean   necks  of   teeth,  salivary   calculus, 
and  green    stain.     (Philadelphia  Dental  Col-        A     maxillary    sinus;    B,    duct  of    Steno;    C, 
lege  Museum.)  parotid  calculus;  E,  submaxillary  gland. 


C,  calculus;  .S.  L.  C,  sublingual  cavity;  S.  L.  G.  L.,  sublingual  gland. 

a  denture  often  accumulates  calculus  in  greater  degree  than  the  side 
used  for  mastication.  This  does  not  occur,  however,  if  the  brusli  be 
ii.sed  properly  and  equally  vigorously  upon  both  sides. 


SALIVARY  CALCULUS 


013 


Burchard  pointed  out  that  irritations  of  various  natures  about 
the  teeth  and  gums  may  by  reflex  action  cause  secretions  of  fluid, 
abnormal  in  quantity  and  quality,  from  both  the  salivary  glands  and 
the  buccal  parietes  (glands  and  gum  margins).  It  is  more  probable, 
however,  that  the  systemic  condition  and  uncleanliness,  together 
with  tooth  form,  is  largely  responsible. 

An  increase  of  oral  fermentation  is  commonly  associated  with  an 
excess  of  calculus  formation,  but  conditions  of  oral  fermentation  may 
be  seen  in  which  but  little  deposit  occurs.  The  mouths  of  many 
children  are  examples  of  this. 

Calculi  harden  with  age.  It  is  commonly  noted  that  soft  calculus 
may  be  readily  removed  with  a  brush.     Calculus  deposited  upon  lower 


Fig.  489 


Right  side,  abrasion  from  overuse;  left  side,  deposits  due  to  stagnation. 

teeth  within  a  week  or  two  after  a  thorough  cleansing  may  be  scraped 
away  as  a  cheesy  mass;  after  a  much  longer  time  it  comes  away  as  a 
hard  scale.  In  very  old  deposits  it  may  be  exceedingly  hard  and 
quite  firmly  attached  to  the  teeth. 

These  clinical  observations  lead  to  the  deduction  that  an  infiltration 
of  calcium  salts  occurs  in  the  dead  organic  stroma  of  the  calculus 
analogous  to  that  occurring  in  dead  or  degenerative  tissue  throughout 
the  body  (calcareous  infiltration  or  degeneration).  Another  theory  is 
possible — i.  e.,  that  a  firmer  chemical  combination  of  the  organic 
and  inorganic  elements  of  the  calculus  occurs,  density  being  thereby 
increased. 

In  the  analyses  furnished  by  StevoTison   (p.  608)  it  will  be  seen 


614 


SALIVARY  AND  SERUMAL  CALCULUS 


that  hardness  is,  in  part  at  least,  due  to  an  increased  proportion  of 
inorganic  elements. 

Theoretically,  subgingival  calculi,  pyogenic  calculi,  and  hemato- 
genic calculi  formed  within  the  unbroken  pericementum  may  derive 
their  organic  material  from  the  secretions  or  necrotic  tissue  of  the  part, 
and  their  inorganic  material  (largely  phosphate  of  calcium,  carbonate 
of  calcium,  and  sodium  biurate)  from  the  serum  of  the  blood  (serumal 
calculus).  In  the  case  of  simple  subgingival  calculus  the  saliva  may 
play  a  part  by  furnishing  the  necessary  calcium  salts,  as  claimed  by 
Peirce,  but  this  does  not  seem  to  be  absolutely  proved,  nor  would  it 
seem  to  be  necessary;  indeed,  in  certain  cases  of  pyorrhea  pockets 
located  about  lower  incisors  in  which  salivary  calculus  might  readily 


Fig.  490 


Fig.  491 


Section  of  a  lower  incisor,  with  a  large  de- 
posit of  salivary  calculus  impinging  upon  and 
causing  inflammation  of  the  gum.     (Black.) 


Section  of  an  upper  molar,  with  deposit  of 
calculus  on  its  buccal  surface,  causing  inflam- 
mation and  absorption  of  the  gum  and  lower 
border  of  the  peridental  membrane  and 
alveolar  wall.     (Black.) 


be  deposited,  and  from  which  both  salivary  and  serumal  calculus  has 
been  thoroughly  removed,  the  serumal  calculus  has  again  collected 
in  quantity,  while  the  salivary  calculus  has  not  been  redeposited. 

Pathological  Effects  of  Salivary  Calculus. — In  contact  with  the  mucous 
meml)raiie  a  salivary  calculus  excites  first  marginal  gingivitis  and 
later  interstitial  gingivitis  and  its  effects.  There  is  sometimes  in 
this  stage  the  wavy,  gnawing,  uneasy  sensation,  associated  with  mild 
inflammation,  and  the  pulp  being  reflexly  irritated  the  teeth  respond 
more  readily  to  thermal  stimuli.  The  gum  margin  is  inflamed, 
and  occasionally  pyogenic  organisms  cause  pus  formation.  The  gum 
margin  recedes  and  coincidently  a  resorption  of  the  alveolar  process 
is  produced.     More  calculus  is  deposited  and  the  process  proceeds 


SALIVARY  CALCULUS 


615 


until  much  of  the  alveolar  support  is  lost.  Microorganisms  no  doubt 
aid  in  the  process. 

The  tooth  is  thus  progressively  loosened,  first  by  inflammation, 
later  by  loss  of  alveolar  process,  moves  about,  and  a  resultant 
mechanical  interstitial  inflammation  of  the  remaining  pericementum 
occurs;  as  a  result  the  membrane  is  thickened  and  the  alveolar 
process  partially  resorbed  (Fig.  490).  Increased  looseness  occurs 
until  the  tooth  drops  out,  unless  mechanically  held  in  place.  As  soon 
as  the  alveolar  loss  is  considerable,  infection  usually  occurs  and 
suppuration  may  be  grafted  upon  the  results  of  mechanical  irritation. 

The  entire  process  may  occupy  but  a  few  years;  in  other  cases 
the  atrophy  of  the  alveolar  walls  is  very  slow. 


Fig.  492 


Fio.  493 


Sectional  illustration  of  a  heavy  deposit  of 
salivary  calculus  on  a  lower  incisor,  with  par- 
tial destruction  of  the  alveolus  of  the  tooth. 
(Black.) 


Sectional  illustration  of  lower  incisor,  with 
deposit  of  salivary  calculus  less  heavy  than 
that  shown  in  Fig.  490,  but  with  greater  de- 
struction of  the  alveolus.     (Black.) 


Prognosis. — The  prognosis  of  this  condition  depends  upon  the  extent 
of  alveolar  atrophy.  If  the  loss  of  support  be  not  so  extensive  as  to 
cause  marked  loosening  of  the  tooth  or  teeth,  the  teeth  may  be  retained 
for  an  indefinite  period  if  they  be  so  attached  to  neighboring  teeth  as  to 
render  them  firm.  If  left  unsupported,  the  pericementum  is  certain  to 
degenerate,  owing  to  the  increased  mobility.  The  alveolar  atrophy  will 
continue,  and  probably  infection  of  the  degenerated  pericementum 
occur.  Redeposit  is  almost  certain  unless  all  morbid  conditions  are 
removed  and  extraordinary  precautions  be  taken  as  regards  clean- 
liness. 

Treatment. — The  treatment  may  be  divided  under  three  heads: 
removal  of  deposits,  correction  of  the  eft'ects  of  their  presence,  and  pre- 


616 


SALIVARY  AND  SERUMAL  CALCULUS 


vention  of  their  recurrence.     The  sole  means  of  removing  salivary 
calculi  should  be  instrumental.     It  is  frequently  recommended  that 


Fig.  494 
3  4 


George  H.  Cushing's  scalers.  The  forms  and  general  character  of  these  scalers 
are  well  shown.  All  the  instruments  except  No.  6  are  Intended  to  be  used  with 
the  push  stroke.  Nos.  1  and  2  are  specially  intended  for  application  to  the  pos- 
terior surfaces  of  lower  incisors;  they  are  also  admirably  adapted  for  removing 
calculus  deposits  below  the  gum  between  molars  and  bicuspids,  and  from  the 
posterior  surfaces  of  the  last  molars.  No.  2  can  be  passed  quite  to  the  extremity 
of  most  roots  with  less  disturbance  to  the  soft  tissues  than  a  thicker  or  more  rigid 
instrument  would  cause.  Nos.  3  and  4  are  for  removing  deposits  at  and  below  the 
gum  between  the  teeth,  particularly  the  lower  front  teeth.  They  can  also  be  easily 
used  upon  the  sides  of  the  roots  of  many  teeth,  being  passed  toward  the  apex  of  the 
root  in  a  line  nearly  or  quite  parallel  with  that  of  the  axes.  No.  5  is  intended  to  be 
passed  between  the  lower  front  teeth  at  or  near  the  gum  and  then  directly  upward, 
to  remove  the  deposits  on  the  proximal  surfaces.  No.  6  is  a  hoe,  and  is  intended  to 
be  passed  quite  to  the  apex  of  the  roots,  where  a  hoe  is  desired. 


Fig.  495 


n 


Scalers. 


mineral  or  some  of  the  organic  acids  be  used  to  soften  the 
deposits  or  facilitate  their  removal.  Anyone  having  seen 
a  case  in  which  a  solution  of  sulphuric  acid  had  been  used 
for  this  purpose  needs  no  further  warning  against  the  appli- 
cation. Acid  solutions  will  certainly  soften  the  deposits,  but 
at  the  same  time  inevitably  cause  a  roughening  of  the  enamel  of 
the  teeth  by  a  solution  of  the  calcium  salts.  To  be  sure,  the  acid 
does  affect  tin;  calculus  more  than   it  alfects   the  enamel,  but  the 


SALIVARY  CALCULUS 

Fig.  496 


617 

Fig.  497 


i;.  ('.  Kirk's  scalers  witli  dentate  ends,  designed  lo  cut  into  calculus  as 
well  as  maintain  tlie  course  of  the  scaler  upon  the  root  side. 


Fig.  498 


Fig.  499 


No.   3  Scaler. 
Fig.  501 


No.  11    Darby- 
Perry  scaler. 


Fig.  502 


Fig.  500 


1  uu 

5  6 

Pyorrhea  scalers  Nos. 
5  and  6,  revised  set.  S.  S. 
White  Dental  Mfg.  Co.'s 
Catalogue.  Intended  for 
use  between  teeth  as  well 
as  for  pyorrhea. 


No.  9   Darby-Perry         No.  35   Darby-Perry 
scaler.  excavator. 


Burton  Lee  Thorpe's  scalers. 


618  SALIVARY  AND  SERUMAL  CALCULUS 

roughened  surfaces  of  the  latter  not  only  invite  wide-spread  deposits 
of  fermentable  material,  but  render  certain  the  more  extensive  accu- 
mulations of  calculi  in  the  future.  After  oral  steriliaztion  the  gross 
deposits  may  be  removed  by  means  of  large,  sickle-shaped  scalers 
and  curved  chisels,  nearly  all  used  with  a  draw  cut  (Fig.  498).  The 
instruments  should  have  sharp  edges  and  be  introduced  beneath  the 
deposits,  so  that  the  gum  be  not  unnecessarily  wounded.  The  scaling 
should  be  continued  until  every  surface  which  can  be  cleansed  by 
these  instruments  is  perfectly  smooth. 

For  the  approximal  surfaces  of  the  lower  anterior  teeth  the  flat- 
bladed  instruments  (Fig.  500)  should  be  used  with  the  push  cut. 
Younger's  pyorrhea  scalers  are  very  useful  (Fig.  513). 

For  the  removal  of  associated  subgingival  calculus  not  too  deeply 
placed  beneath  the  gum  a  No.  35  Darby-Perry  excavator  is  of  almost 
universal  utility.  It  is  used  with  the  draw  cut  for  the  most  part.  A 
pair  of  them  may  be  employed  and  made  safe-sided  by  rounding  one 


Moose-hide  wheels, 

edge  if  desired  to  avoid  injury  of  the  gum  margin.  The  back  of  the 
instrument  may  be  sharpened  to  an  edge  for  a  push  cut.  All  of  the 
calculi  visible,  and  all  that  can  be  detected  by  their  roughness,  are 
thoroughly  detached  and  scraped  away  by  these  instruments.  The 
surfaces  of  the  teeth  are  next  cleansed  with  pumice  made  into  a  paste 
with  glycerin  to  prevent  spattering.  The  paste  is  applied  to  the  sur- 
faces of  the  teeth  with  rubber  cups,  or  Abbott's  or  Robinson's  brush 
wheels,  which  are  used  to  cleanse  the  labial,  buccal,  and  such  lingual 
faces  of  the  teeth  as  they  will  reach  (Figs.  504  to  509).  The  gum 
should  not  be  injured.  The  lingual  surfaces  of  upper  and  lower 
incisors  are  cleansed  with  moose-hide  wheels  and  wheel  brushes;  a 
finishing  bur^  is  useful  in  the  removal  of  thinly  distributed  hard 
calculi  on  lingual  and  occlusal  surfaces,  especially  in  mouths  of 
smokers. 

The  approximal  surfaces  of  the  teeth  are  cleansed  with  fine  linen 
tape  or  floss  silk  charged  with  the  pumice  paste.  More  inaccessible 
parts  require  the  use  of  an  orange-wood  point  mounted  in  a  Jack 

1  Guilford  Lectures. 


SALIVARY  CALCULUS 


619 


porte-polisher.    Hickory  shoe  pegs  are  useful.    It  is  advisable  to  repeat 
the  polishing  with  precipitated  chalk  and  the  same  carriers. 


Fig.  504 


Fig.  507 


Fig.  508 


Fig.  509 


.V*,-  m 


After  cleansing,  the  associated  gingivitis  should  be  re- 
duced and  the  parts  kept  sterilized  while  healing  bv  means 
of  an  antiseptic  astringent  mouth  wash.     (See  Gingivitis.) 
If  If  desired,  the  operation  may  be  divided,  the  gross  de- 

V  posits  and  subgingival  calculus  being  removed  at  the  first 
sitting.  After  a  few  days'  use  of  the  mouth  wash  the 
stains  and  bacterial  plac[ues  upon  the  teeth  and  any  overlooked  de- 
posits may  be  removed.  Tincture  of  iodine  painted  over  the  teeth 
brings  the  deeper  stains  of  the  collections  into  prominence,  as  does 
also  a  solution  of  potassium  permanganate. 


620 


SALIVARY  AND  SERUMAL  CALCULUS 


Register  states  that  a  forcible  spray  of  1  per  cent,  hydrogen  dioxide 
used  after  the  appHcation  of  tincture  of  iodine  will  soften  the  stains 
and  render  them  more  readily  removable. 

The  smoother  the  surfaces  of  the  teeth  are  made,  the  longer  the 
redeposition  of  calculi  will  be  delayed. 

It  is  a  wise  measure  to  cleanse  the  teeth  before  any  long  series  of 
operations  is  undertaken,  and  as  a  prophylactic  measure  in  the  combat 
with  caries  and  pyorrhea  alveolaris  the  operation  should  be  frequently 
performed.  Indeed,  the  teeth  should  be  cleansed  frequently,  so  that 
it  may  not  be  necessary  to  remove  actual  salivary  calculus,  except 
in  those  cases  in  which  it  collects  with  abnormal  rapidity.  (See 
Prophylaxis  of  Caries  and  of  Pyorrhea  Alveolaris.) 

In  cases  of  very  rapid  recurrence  of  salivary  deposits,  evidence  of 
an  associated  systemic  condition  should  be  sought.  In  this  direction 
sialosemeiology  and  urinalysis  may  develop  data  worthy  of  attention. 
The  systemic  condition,  if  recognizable,  should  receive  appropriate 
treatment. 

SUBGINGIVAL   CALCULUS. 

By  subgingival  calculus  is  meant  that  form  of  deposit  which  occurs 
beneath  the  free  gum  margin  and  between  it  and  the  tooth.  The 
deposits  consist  of  small  scales  or  granules,  usually  quite  smooth  and 
much  darker  (olive  green)  than  salivary  calculi  (Fig.  510). 


Fig.  510 


Fig.  511 


A,   suliKinKival  calculus;   /?,  receding  perioe- 
nrientuin. 


Resorption  of  the  septum  of  bone  and 
receHsion  of  the  gum  between  the  central  and 
lateral  incisors,  caused  by  dei)()sits  of  scnnnal 
calculus  under  tlie  gingivic.     (Black.) 


Composition.^ — 'I'h(-'y  consist  mainly  of  calcium  phosphate  com- 
bined with  undetermined  organic  substances.     (See  p.  G08). 

Cause  and  Pathology .^ — It  is  probable  that  some  degree  of  marginal 
gum  irritation  first  occurs,  though  many  cases  of  an  apparently  healthy 


SUBGINGIVAL  CALCULUS  621 

gum  with  a  scale  of  calculus  beneath  it  are  seen.  Whether  the  irritation 
arises  through  fermentations  about  the  unclean  necks  of  the  teeth  or 
as  the  result  of  an  efl'ort  upon  the  part  of  the  gum  margin  to  eliminate 
waste  products  from  the  system  is  not  absolutely  certain. 

The  theory  most  tenable  is  that  uncleanliness  exists;  fermentation 
of  the  mixed  marginal  eolkction  and  gum  secretion  occurs,  the  gum 
secretion  containing  calcium  salts;  these  are  precipitated  with  some 
organic  matter,  forming  a  calculus.  Fig.  255  shows  a  calculus  or 
unerupted  tooth  root  showing  that  the  bloo<l  contains  the  elements 
necessary  for  its  formation  under  localized  irritation. 

Talbot  has  shown  that  a  natural  pocket  may  exist  at  some  aspect 
of  the  gingival  space  which  is  capable  of  harboring  collections  of 
foreign  material.  The  normal  gum  margin  closely  approximates  the 
tooth  and  has  an  apparent  protective  influence  over  the  portion  if 

Fig.  512 


The  alveoli  irreparably  destroyed  by  calcic  inflammation.     (Black.) 

covers.  For  some  reason,  such  as  a  lack  of  normal  friction  or  the 
presence  of  microbic  plaques  just  above  it,  the  gum  may  lose  its 
normal  tone  and  the  calculus  deposition  be  favored.  Its  secretion  is 
also  probably  altered  in  quality. 

Effects  and  Symptoms. — The  direct  effects  are  exerted  upon  the  gum 
margin.  The  mechanical  irritation  may  cause  the  gum  antl  alveolar 
process  to  undergo  resorption,  the  calculus  being  exposed. 

At  times  this  resorption  is  accompanied  by  evident  marginal  inflam- 
mation, at  others  the  gum  margin  has  a  normal  color,  but  the  resorbing 
portion  is  sharply  defined  by  a  fine  line  (or  crease)  from  the  normal 
gum  tissue.  In  a  more  advanced  stage  this  demarked  portion  appears 
sunken  or  atrophied  and  may  have  a  sort  of  semihyaline  redness 
characteristic  of  the  inflammation.  At  times  the  gum  margin  appears 
everted.  If  the  deposit  occur  on  only  one  side  of  a  root  the  gum 
resorption  may  be  confiiud  to  that  sitle. 


622 


SALIVARY  AND  SERUMAL  CALCULUS 


The  lingual  root  of  an  upper  molar  is  often  exposed  for  a  con- 
siderable portion  of  its  length  by  successive  deposits  of  calculi.  The 
same  is  true  in  other  situations,  notably  upon  the  labial  surface  of  a 
lower  incisor. 

Fig.   513 


9  10  II     12  13  14  15 

Younger's  new  set  of  pyorrhea  instruments.     (Revised  by  Dr.  Robert  Good.) 

Fig.  514 


Tompkins'  pyorrhea  scalers. 


If  the  deposit  be  generally  distributed  about  the  neck  of  the  tooth 
the  resorption  is  more  ecjualized. 

In  some  cases  the  bifurcation  of  roots  may  be  exposed  and  calculi 
deposit  in  that  situation. 


PYOGENIC  CALCULUS  623 

In  some  cases  the  gum  margin  becomes  simply  atonic  or  passively 
congested  and  is  pushed  away  from  the  teeth  by  large  masses  of  the 
calculus,  which  undergo  lateral  accretion.  It  appears  as  a  flabby, 
thickened,  loosened  gum  margin,  which  readily  draws  about  the  necks 
of  the  teeth  if  the  calculus  be  removed. 

Finally,  pyogenic  infection  may  occur  about  the  calculus  and  the 
symptoms  of  pyorrhea  alveolaris  be  implanted.  \Mien  this  is  estab- 
lished, calculi  may  be  deposited  farther  up  the  side  of  the  root. 

Treatment. — The  calculus  should  be  removed  by  means  of  delicate 
scalers  used  with  either  the  push  or  draw  cut,  as  most  convenient, 
after  which  astringent  antiseptic  mouth  washes  shoidd  be  prescribed. 
The  subsetjuent  frequency  of  removal  and  oral  prophylaxis  are  of 
great  importance.  Figs.  513  and  514  show  convenient  forms  also 
useful  for  the  deeper  pyorrhea  pockets. 


PYOGENIC  CALCULUS. 

Pyogenic  calculus  is  that  form  of  serumal  calculus  which  is  deposited 
at  parts  of  the  tooth  root  over  which  pus  more  or  less  continually 
flows.     Talbot  has  shown  that  pus  is  rich  in  calcium  phosphate. 

In  chronic  apical  abscess  the  root  end  may  become  encrusted  with 
it,  and  in  those  cases  in  which  apical  abscess  discharges  along  the 
pericemental  tract  it  is  common  to  find  over  the  area  fine  granular 
deposits  which  vary  in  color  from  a  light  yellow  to  a  reddish  brown. 

The  same  is  true  of  active  pyorrhea  pockets. 

This  calculus  prevents  the  healthy  ap])osition  of  the  gum  tissue  to 
the  roots,  probably  because  of  its  irritant  and  infective  nature  (Fig. 
441). 

Treatment. — All  such  calculi  should  be  removed  by  whatever  means 
possible,  which  may  necessitate  scraping  the  root  end  or  its  side,  or 
even  the  amputation  of  the  apical  end  of  the  root.  In  some  cases 
25  per  cent,  sulphuric  acid  may  dissolve  it.     (See  p.  547.) 


HEMATOGENIC  CALCULUS  (Syn.  SANGUINARY  CALCULUS). 

This  form  of  senmial  cakuhis  occurs  in  the  so-called  gouty  peri- 
cementitis, a  form  of  pericemental  abscess. 

It  may  occur  in  the  absence  of  apical  abscess  or  a  primary  pvorrhea 


624  SALIVARY  AND  SERUM AL  CALCULUS 

alveolaris,  and,  therefore,  at  points  not  acted  upon  by  saliva  or  pus; 
hence  it  must  be  deposited  by  the  blood  through  the  lymph. 

^Nliller^  has  offered  a  satisfactory  evidence  of  this  in  a  description 
of  a  case  of  impacted  cuspid  well  embedded  in  the  bone,  and  not  in 
any  way  exposed  to  either  saliva  or  pus  influence  except  that  at  a 
point  over  the  cusp  the  gum  underwent  suppuration  for  a  short  time. 
The  crown  had  undergone  resorption,  showing  local  irritation,  and  an 
olive-green  calculus  had  formed  upon  the  middle  third  of  the  root. 
Cases  of  pericemental  abscess  have  been  noted  opening  upon  the  gum 
face  and  presenting  dark  green  calculi  upon  the  root  in  that  situation 
(Fig.  255).     (See  Pericemental  Abscess.) 

Peirce  found  in  such  deposits  a  proportion  of  sodium  urate  as  shown 
by  the  murexide  test  and  the  cases  associated  with  goutiness  of  the 
patient. 

\Miile  such  deposits  may  not  cause  immediate  irritation,  they  may 
in  time  excite  inflammation  and  necrosis  of  tissue,  resulting  in  a  dis- 
charge of  glairy  material  representative  of  the  condition.  This  form 
of  dental  disease  will  be  further  discussed. 

1  Dental  Cosmos,  1901. 


CHAPTER    XXIV. 
PYORRHEA  ALVEOLARIS. 

While  the  term  pyorrhea  alveolaris  implies  but  one  symptom 
common  to  several  distinct  varieties  of  disease  of  the  pericementum, 
that  of  a  flow  of  pus  from  the  alveolus,  it  is  generally  understood  as 
a  term  descriptive  of  degenerative  conditions  which  have  some  distinc- 
tive features;  these  are  a  progressive  loosening  of  the  teeth  attended  by 
a  loss  of  the  retentive  structures,  alveolar  walls,  and  pericementum,  the 
loosening  of  the  teeth  being  in  a  majority  of  cases  attended  by  a  flow 
of  pus  from  the  margin  of  the  affected  alveolus,  and  by  deposits  of 
calculi  upon  the  sides  of  the  denuded  roots.  The  disease  ceases  spon- 
taneously with  the  loss  of  the  teeth,  the  resoi-ption,  loss,  or  atrophy 
of  the  alveolar  wall  being  arrested  at  any  period  of  the  disease,  if  the 
affected  tooth  be  extracted. 

Causes. — The  several  clinical  varieties  of  this  disorder  all  seem  to 
be  associated  with  an  obvious  infection,  which  in  turn  has  found  a 
favoring  condition  in  a  degenerative  state  of  the  pericementum  or 
gum  margin  of  one  or  more  teeth.  While  this  is  probably  true, 
investigations  in  this  direction  have  proved  negative  in  so  far  as  the 
determination  of  a  specific  bacterium  is  concerned. 

Galippe  and  Malassez,  INIiller,  Black,  Talipot,  Goad  by.  Younger, 
Cook,  and  others  have  all  failed  to  definitely  isolate  such  a  specific 
bacterium.  The  closest  approach  to  a  demonstration  yet  made  was 
the  determination  by  Kirk  of  the  presence  of  a  pure  culture  of  the 
Diplococcus  pneumoniae  in  a  few  cases  of  freshly  opened  pericemental 
abscesses  (which  see). 

The  investigations  of  Goadby,  however,  do  not  confirm  this  as  a 
cause  of  pyorrhea  alveolaris  in  general,  but  rather  point  to  the  prob- 
ability that  the  cause  may  be  found  among  other  oral  bacteria,  possibly 
thread  forms  or  some  of  the  blastomycetes.  Talbot  believes  the 
ordinary  pyogenic  cocci  to  be  the  cause  of  the  pus  production. 

Curtis^  believes  obstinate  cases  of  the  disease  to  be  either  caused 
by  or  aggravated   by  tertiary  syphilis.     He    bases   his   belief  upon 

'  Dental  Cosmos,  1901. 
40 


626  PYORRHEA  ALVEOLARIS 

observations  of  fresh  blood  which,  he  states,  upon  the  authority  of 
Dr.  Robert  L.  Watkins  (New  York  City),  contains  syphihtic  spores. 

"Egg-skin"  eschar  is  the  oral  pathognomonic  sign. 

The  local  infection  in  nearly  all  cases  is  of  so  mixed  a  type  as  to  render 
it  at  present  uncertain  whether  the  liquefaction  of  the  peridental  mem- 
brane, etc.,  is  due  directly  to  the  pyogenic  organisms  present  in  the 
pus  formed  or  to  other  oral  bacteria  of  uncultivable  type  which  may 
initiate  the  process,  after  which  pyogenic  organisms  may  enter  and 
form  pus.  The  fact  that  pyorrhea  alveolaris  is  seldom  found  fully 
established  before  thirty  years  of  age,  but  is  common  after  that  period, 
and  that  it  occasionally  occurs  in  youth  or  even  in  childhood  in  associa- 
tion with  some  pronounced  systemic  state  or  disease,  strongly  indicates 
a  systemic  factor  in  the  more  pronounced  forms  of  the  disease.  It  is 
probable  that  the  various  systemic  diseases — e.  ^.,  rachitis  in  childhood, 
Bright's  disease,  auto-intoxications,  anemia,  or  neurasthenia  in  adults, 
etc. — ^have  a  degenerative  influence  over  the  pericementum  in  one  of 
two  ways:  1.  By  introducing  the  factor  of  retention  of  normal  or 
abnormal  waste  metabolic  products  within  the  body  fluids  which, 
presented  as  food  to  the  pericemental  cells,  act  as  irritants  (auto- 
intoxication). 

2.  Through  a  possible  deprivation  of  the  pericemental  tissue  of 
necessary  nutritive  material  (tissue  starvation) — e.  g.,  as  in  anemia. 

It  is  a  well-known  fact  that  peripheral  nutrition  is  disturbed  by 
systemic  conditions — e.  g.,  the  rapid  falUng  out  of  quantities  of  the 
hair  during  periods  of  excessive  drain  upon  the  system,  as,  for  example, 
during  lactation. 

At  other  periods  no  such  result  may  be  noted.  The  presumption  is 
that  a  disturbed  peripheral  nutrition  or  circulation  from  any  cause 
renders  the  part  affected  less  resistant  to  the  action  of  the  micro- 
organisms. 

The  investigations  of  Michaels  and  Kirk  upon  the  composition  of 
saliva  in  various  systemic  states  throws  much  hght  upon  the  possibility 
of  the  presence  of  the  before-mentioned  irritants  in  the  blood  fluid. 
Kirk^  reports  the  finding  of  quantities  of  sodium  oxalate  in  the  urine 
of  certain  patients  suffering  from  malnutrition  and  neurasthenia. 
These  later  followed  by  the  appearance  in  the  saUva  and  urine  of 
calcium  oxalate.  These  are,  of  course,  derived  from  the  blood.  The 
presencf;  of  sodium  urates  in  the  })lood  in  gout  is  well  estabhshed. 
Using  these  substances,  then,  as  a  foundation  for  argument,  it  is  seen 

'  Dental  Cosmos,  July,  1903. 


PYORRHEA  ALVEOLARIS  627 

that  lu)  reason  exists  why  these  (and  other  waste  pro(hicts  as  well) 
should  not  float  through  the  capillaries  and  lymph  channels  or  even 
the  glands  of  the  pericementum,  and  produce  irritation  which  may  be 
followed  by  atrophic  or  hyperemic  changes  in  that  tissue.  These 
changes  are  well  known  to  lead  to  degeneration,  and  degeneration 
lessens  resistance.  At  this  point  the  microorganisms  produce  active 
effects  which  previously  are  resisted.  In  this  connection  the  fibroid 
degeneration  of  the  pericementum  due  to  age,  demonstrated  bv  Ilope- 
well-Smith,  should  have  some  consideration  as  a  predisposing  cause 
at  the  proper  age.     (See  also  ]).  598.) 

It  is  not  to  be  supposed  that  local  causes  are  not  competent  to  pro- 
duce pericemental  degenerations — e.  g.,  such  causes  as  malocclusion, 
overuse,  abuse,  and  disuse  of  teeth;  the  lack  of  friction  necessary  to 
maintain  the  normal  tone  of  the  gums;  the  excess  of  friction  in  some 
cases. 

The  presence  of  fermentable  material  about  the  necks  of  the  teeth, 
particularly  those  of  the  narrow-necked  variety,  causing  the  precipi- 
tation of  calculus,  in  short,  any  of  the  causes  of  interstitial  gingivitis 
or  pericementitis,  may  excite  the  degenerations  following  chronic  irri- 
tation, and  thus  favor  the  development  of  the  bacteria  producing 
pyorrhea. 

It  has  been  argued,  notably  by  D.  D.  Smith,  that  if  the  teeth  be 
frequently  thoroughly  cleansed  of  all  deposits  of  all  sorts,  the  pyorrhetic 
conditions  will  be  cured.  The  success  which  seems  to  attend  the  use 
of  the  rr-rays  and  high-frequency  electric  current  in  this  condition  is 
also  argument  that  the  cause  may  be  killed  out  by  local  treatment 
alone.  It  does  not  follow,  however,  that  a  cure  by  removal  of  a  cause 
implies  a  lack  of  predisposition  on  the  part  of  the  tissues  of  a  part  or 
individual.  The  tendency  in  some  cases  to  relapse  unless  the  cause 
be  continually  removed  is  a  proof  of  this  fact. 

It  has  been  shown,  on  the  other  hand,  that  intelligent  attention  to 
systemic  conditions  has  been  followed  by  amelioration  or  in  some  cases 
even  cure  of  the  pyorrhea  when  local  treatment  alone  (apart  from 
constant  attention)  has  failed — /.  e.,  an  increased  resistance  of  the 
tissues  to  the  bacteria  present  has  been  brought  about  by  the  sys- 
temic treatment. 

The  argument  that  pyorrhea  alveolaris  is  of  purely  local  origin, 
because  it  disappears  after  the  tooth  is  extracted,  is  no  more  sound 
than  would  be  the  argument  that  gout  in  the  great  toe  is  of  local  origin 
because  it  disappears  with  the  amputation  of  tlic  leg.     Pvorrhea  is 


628  PYORRHEA  ALVEOLARIS 

a  disease  of  the  dento-alveolar  joint  (the  pericementum),  and  extrac- 
tion ehminates  that  joint. 

It  is  also  argued  that  the  local  infection  is  competent  to  produce 
not  only  the  gingivitis,  but  also,  by  the  production  of  toxins,  either  in 
the  oral  cavity  or  at  some  point  in  the  ahmentary  canal,  to  produce 
the  systemic  malnutrition. 

"\Mien  the  long  continuance  of  oral  infection  is  considered,  this  view 
is  entitled  to  great  respect,  but  the  general  predisposition  must  again 
be  a  factor  in  the  advance  of  the  disease. 

In  brief,  it  may  be  stated  that  the  infectious  nature  of  pyorrhea 
alveolaris  is  becoming  more  established,  albeit  not  yet  fully  scientifi- 
cally proved,  and  that  the  causes  require  a  local  predisposition  for  their 
action.  This  local  predisposition  may  be  the  outcome  of  local  sources 
of  irritation  and  degeneration  alone  or  be  produced  by  waste  products 
floating  in  the  blood  stream,  etc. 

Chnically,  fully  estabHshed  cases  of  pyorrhea  alveolaris  may  be 
divided  into  three  classes:  (1)  Cases  associated  with  a  primary  gin- 
givitis and  with  the  formation  of  hard,  scaly,  dark,  annular  calculi 
beneath  the  gum  margin  (subgingival  calculus),  the  pockets  not 
usually  extending  far  beyond  the  deposits;  (2)  cases  beginning  with  a 
marginal  gingivitis  and  apparently  not  dependent  upon  the  association 
with  calculus,  though  frequently  complicated  by  it;  (3)  cases  having 
an  apparent  origin  at  some  point  between  the  gingival  margin  and  the 
apical  tissue,  the  gingival  margin  at  first  bein^  apparently  intact. 

It  is  probable  that  the  infecting  agents  in  these  types  differ  in 
their  nature,  or  that  in  the  event  that  they  may  be  proved  to  have  a 
similar  origin  the  tissues  react  differently  to  them,  either  partially 
resisting  them,  forming  calculus  as  a  result  of  the  irritation,  or  rapidly 
giving  way  to  them,  permitting  a  deep  action. 

In  the  absence  of  known  causes  the  conditions  may  be  divided 
according  to  their  clinical  expressions. 

In  the  consideration  a  pus  flow  due  to  apical  abscess,  lateral  abscess 
upon  a  perforation,  or  that  due  to  obvious  salivary  calculus  is  excluded. 
(For  these,  see  under  proper  headings.) 

PYORRHEA   ALVEOLARIS  BEGINNING  AS  A  MARGINAL   GINGI- 
VITIS AND  ASSOCIATED  WITH    SUBGINGIVAL  CALCULUS. 

Causes. — The  causes  of  this  condition  are  those  predisposing  and 
exciting  causes  of  marginal  gingivitis  which  have  been  described. 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS       629 

(See  p.  592.)  Several  local  factors  have  to  be  considered  in  this 
connection:  (1)  The  marginal  infection;  (2)  the  irritative  effects  of  any 
calculus  that  may  be  formed;  (3)  the  deep  infection  by  pyo<i;enic 
organisms;  (4)  the  modification  of  the  progress  of  the  disease  by  the 
attendant   loosening  of  the  teeth  and  death  of  the  pulp. 

Clinical  History,  Pathology,  and  Symptoms. — There  is  usually  an 
unclean  condition  of  the  teeth;  infection  exists  either  in  tenacious 
films  of  bacteria  attached  to  the  necks  of  the  teeth  and  recpiiring 
reasonably  close  observation  for  their  detection,  or  in  masses  of 
detritus  readily  noticeable.  Subgingival  calculus  is  obviously  pres- 
ent (Fig.  518). 

Fig.  515 


Serumal  calculus,  sliowing  stalactite-likp  formations.     (Talbot.) 

The  gum  margin  may  be  atrophied  or  be  inflamed ;  or  it  may  have 
a  fairly  normal  appearance.  "When  the  gum  margin  is  pressed  upon, 
pus  may  be  scjueezed  out  in  variable  quantity. 

It  is  assumed  thatjhe  local  infection  brings  about  fermentation  at 
a  point  beneath  the  gum  margin,  and  that  formation  of  subgingival 
calculus  occurs,  followed  by  pyogenic  infection  and  pus  formation. 

The  gum  may  now  be  resorbed  either  with  apparently  normal  bulk 
or  the  margin  may  be  everted  and  thickened  into  a  cord-like  margin 
which  is  either  of  normal  color  or  inflamed;  the  shrinkage  of  the  gum 
causes  the  expo.sure  of  the  calculus  (Fig.  510).     Tn   this  manner  the 


630 


PYORRHEA  ALVEOLARIS 


Fig.  516 


bifurcations  of  the  roots  may  be  uncovered  and  calculi  be  deposited  in 
that  situation.  The  resorption  may  only  be  confined  to  one  side  of  a 
root  and  be  the  result  of  several  successive  depositions  which  may 
remain  when  the  gum  recedes,  or  which  may  be  removed  and  again  be 
deposited.  In  this  way  the  side  of  the  root  may  be  exposed  nearly  to, 
and  in  some  cases  quite  to,  the  apex.  In  such  cases  the  pus  pockets 
may  not  be  deep  and  the  pus  formed  may  readily  be  washed  away. 
Instead  of  this  the  pericementum  may  be  progressively  destroyed  by 
suppuration  and  the  gum  margin  remain  prac- 
tically intact.  In  these  cases  the  pus  flow  is 
more  abundant,  a  deep  pocket  is  formed,  extend- 
ing a  third  or  even  two-thirds  or  more  of  the 
length  of  the  root  (Fig.  516).  It  is  common  to 
find  beads  of  calculus  deposited  along  the  side 
of  the  root  and  presumably  of  serumal  origin. 
(See  p.  507.) 

These  inflammatory  disturbances  necessarily 
involve  an  interstitial  gingivitis  or  infiltration 
of  leukocytes  into  the  interstitial  connective 
tissue  of  the  gum.  As  pointed  out  by  Talbot, 
resorption  of  various  kinds  and  at  times  con- 
structive changes  accompany  such  an  inflam- 
mation. (See  Interstitial  Gingivitis.)  Endarteritis  is  also  noted. 
These  results  are  noted  in  connection  with  this  variety  of  pyorrhea 
alveolaris.  In  the  early  stages  of  the  disease  the  probe  usually  fails 
to  discover  uncovered  alveolar  bone,  although  it  may  do  so.  If  not 
uncovered  its  loss  is  due  to  resorption;  if,  however,  necrotic  and  bare 
alveolar  bone  be  found,  it  is  undergoing  a  molecular  necrosis  under 
the  influence  of  the  pyogenic  organisms. 

In  some  cases  the  pericementum  may  be  destroyed  at  the  cervical 
third  of  the  root,  the  alveolar  process  may  be  resorbed  on  its  inner 
surface,  and  an  accompanying  constructive  irritation  may  cause  the 
deposition  of  bone  upon  the  outer  aspect  of  the  alveolar  process;  the 
gum  margin  is  also  thickened  by  cell  proliferation.  The  condition 
imparts  the  appearance  of  hypertrophy  of  the  gum  and  gum  margin 
(Fig.  518).  The  inflammation  of  the  pericementum  may  become 
general  and  the  attendant  swelling  forces  the  tooth  into  malocclusion 
with  its  antagonist.  The  mechanical  factor  is  now  introduced  and 
the  extrusion  increases  gradually  or  even  raj)idly. 

When  ab(jut  one-half  or  more  of  the  root  has  been  stripped  of 


Pyorrhea  pockets.  Me- 
sial root  of  molar  largely 
denuded.  Treated  by  am- 
putation.    (Price.) 


PYORRHEA   ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS      031 


Fig.  517 


pericementum  and  deprived  of  alveolar  support,  looseness  and  extru- 
sion of  the  tooth  become  marked. 

The  advance  of  the  disease  now  becomes  more  rapid;  the  undue 
mobility  and  malocclusion  of  the  tootli  excite  an  inflammatory 
reaction  beyond  the  directly  infected 
part,  so  that  soreness  and  looseness  are 
further  increased.  Extraction  at  the 
later  stages  reveals  a  thickened  apical 
pericementum  as  the  sole  attachment 
to  the  bone.  After  the  looseness  of  the 
tooth  becomes  marked,  the  pulp  of  the 
tooth  undergoes  h^'peremic  changes, 
reacts  to  thermal  stimuh,  and  is  often 
killed  by  strangulation  of  its  vascular 
supply.  Pulp  nodules  often  are  formed 
before  its  death.  Reflex  symptoms  may 
occur  at  this  stage.  Infection  of  the  dead 
pulp  readily  occurs,  and  septic  apical 

pericementitis  arises.  The  symptoms  of  the  latter  condition  are 
modified,  according  to  the  facility  with  which  the  pus  finds  vent  along 
the   degenerating  pericementum.     The   disease   proceeds   until   the 


Secticin  of  an  upper  inoisor,  sliowing 
at  a,  a  a  deposit  of  serunial  calculus 
within  the  free  margin  of  the  gum. 
(Black.) 


Fig.  518 


Fig.  519 


Section  of  an  upper  incisor,  showing  de- 
struction of  the  peridental  membrane  and 
eversion  of  the  alveolar  wall,  with  thickening 
of  it.s  border:  a.  serunial  calculus;  b,  (liick- 
ened  border  of  the  alveolar  wall;  c,  pus 
cavity.     (Black.) 


Section  of  an  upper  molar  with  its  alveolus, 
etc.,  showing  deposit  of  seminal  calculus 
under  the  gingival  borders:  a,  a,  serumal  cal- 
culus.    (Black.) 


affected  tooth  or  teeth  are  cast  out,  the  alvt  cilar  walls  and  pericementum 
having  entirely  atro})hied.  The  disease  cea.ses  with  the  lo.ss  of  the 
att'ected  teeth,  leaving  a  flattened  or  absent  alveolar  ridge  covered  by 
a  mass  of  more  or  less  spongy  gum  tissue. 


632 


PYORRHEA  ALVEOLARIS 


The  duration  of  this  disease  may  be  months  or  years,  and  a  number 
of  teeth  may  be  affected  at  once.  A  general  subcatarrhal  condition 
of  the  mouth  usually  attends  the  disease.  The  presence  of  pus  often 
imparts  to  the  breath  a  pecuhar,  sweetishly  fetid  odor  which  may, 
however,  be  masked  by  an  odor  of  putrefaction. 

In  a  number  of  cases  of  deep  pyorrhea  pockets  an  infection  of  the 
alveolar  structure,  or,  at  least,  of  the  tissue  remaining  over  the  deepest 
portion  of  the  pocket,  may  occur,  and  an  abscess  form  which  dis- 


FiG.  520 


Inflammation  of   pericementum,   endarteritis  obliterans,  Talbot's  case.     (Latham.) 

charges  by  a  fistula  through  the  labial  or  lingual  aspect  of  the  gum. 
It  is  to  be  regarded  as  an  abscess  secondary  to  a  primary  pyorrhea 
alveolaris.  The  passage  of  a  silver  probe  through  the  two  sinuses  at 
once  will  reveal  this  (Fig.  521).  In  a  tooth  treated  for  apical  abscess 
such  a  pyorrhea  pocket  existed,  and  doubt  arose  as  to  the  cause.  The 
fact  that  it  was  near  the  gum  margin  and  the  probe  could  not  be 
passed  into  a  sinus  leading  to  a  root  was  considered  evidence  of  abscess 
secondary  to  pyorrhea.  Evacuation  and  antisepsis  were  sufHcient  to 
effect  a  cure. 


PYORRHEA   ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     033 

In  one  case  of  pyorrhea  alveolaris  of  the  variety  under  consideration 
the  pocket  existed  upon  the  niesiohuccal  aspect  of  a  right  lower  third 
molar.  The  second  and  first  molars  were  absent.  The  pus  dissected 
away  the  periosteum  of  the  bone  and  formed  a  large  abscess  over  the 
entire  area  of  bone  between  the  third  molar  and  second  bicuspid. 
After  evacuation  of  the  abscess,  the  probe  was  passed  through  it  to 
the  pyorrhea  pocket  (Fig.  522).  Another  expression  occasionally 
occurs.  The  infection  travels  via  the  natural  channels  in  the  peri- 
cementum from  the  ])yorrhea  pocket  to  a  deeper  point  in  the  perice- 
mentum (for  example,  to  a  point  one-quarter  inch  or  more  below — 
producing  what  is  called  a  pericemental  abscess.  The  tissue  between 
may  seem  unbroken  and  the  fistula  may  seem  hke  that  associated 
with  chronic  apical  abscess.  Fig.  523  will  illustrate  the  maimer  in 
which  this  may  occur. 


Fig.   521 


Fig.  522 


Gingival  abscess  secondary  to  pyorrhea 
alveolaris:  C,  calculus  in  pyorrhea  pocket; 
/',  fistula  leading  to  pocket  PP;  B,  bone  on 
lingual  side. 


Diagram  of  abscess  secondary  to  pyorrhea 
alveolaris  (see  text):  PP,  pyorrhea  pocket; 
AC,  cavity  of  secondary  abscess;  B,  bone. 


While  dental  caries  may  occur  with  pyorrhea  alveolaris,  it  is  usual 
to  find  the  teeth  of  the  most  highly  organizetl  structure.  The  pulp 
tissue  is  usually  increased  in  density,  and  there  is  a  tendency  to  the 
constructive  changes,  secondary  dentine,  nodules,  etc.,  and  the  inevi- 
table degenerative  changes  following  these  diseases. 

It  has  been  contended  that  these  pulps  are  responsible  in  a  measure 
for  the  pyorrhetic  condition,  and  it  is  possible  that  they  may,  by  reflex 
action,  influence  the  tissue  nutrition  of  the  pericementum  and  gum 
margin,  though  the  contrary  process  is  more  than  probable,  as 
pyorrhea  frequently  causes  a  pulp  hyperemia  which  subsides  with  the 
cure  of  the  pocket.  If  the  pulps  be  degenerated,  which  is  likely  in 
very  loose  teeth  or  deep  pockets,  their  removal  aids  the  cure  of  the 
disease  by  diverting  the  blood  they  receive  into  the  pericemental 


634 


PYORRHEA  ALVEOLARIS 


bloodvessels.     This  probably  counterbalances  the  effects  of  the  end- 
arteritis obliterans.     (See  Interstitial  Gingivitis.) 

It  is  also  true  that  calculus  does  not  seem  to  form  as  readily  upon 
a  devitalized  tooth  as  upon  one  containing  a  vital  pulp;  it  does  form 
at  times,  however. 

Fig.  523 


Pericemental  abscess  associated  with  a  pyorrhea  pocket.     (V.  A.  Latham.) 

Diagnosis. — The  diagnosis  is  easily  made  when  the  disease  is  estab- 
lished by  observance  of  the  phenomena  just  described.  In  difficult 
cases  with  pocket  approaching  the  apex  or  l^ifurcation  a  skiagraph 
may  be  necessary  for  accurate  determination  of  the  extent  of  the 
disease.  A  persistent  gingivitis  with  an  exaggeration  of  the  space 
between  the  tooth  and  gum  margin  means,  as  a  rule,  a  future 
pyorrliea.  The  same  is  true  of  a  receding  gum  margin  constantly 
associated  with  an  uncleanly  tooth  cervix.  The  causes  of  the  con- 
dition are  to  l)e  removed  and  the  patient  cautioned  to  seek  frequent 
dental  attention  as  a  prophylactic  measure. 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     C35 

Prophylaxis. — As  outlined  above,  the  prevention  of  pyorrhea  areo- 
laris of  the  first  class  involves  the  removal  of  the  local  and,  if  possible, 
the  systemic  causes  of  the  gingivitis,  and  the  systematic  cleansing  of 
the  teeth  at  short  intervals.  The  daily  use  of  the  tooth-brush  and 
antiseptic  powders  and  washes  by  the  patient  is  also  important. 

D.  D.  Smith  advises,  for  this  class  of  cases,  a  thorough  cleansing 
once  a  month,  or  at  first  even  oftener.  The  cleansing  is  to  be  done 
with  an  orange-wood  point,  grasped  in  a  Jack  porte-polisher  and 
charged  with  pumice  paste.  The  local  sources  of  gum  infection 
are  thus  continually  removed  and  the  gums  stimulated  by  the 
mechanical  irritation  with  the  wood  point. 

Treatment. — ^The  treatment  of  well-established  pyorrhea  alveolaris 
of  the  first  class  is  to  be  considered  under  three  headings:  (1)  The 
removal  of  pus,  calculus,  and  bacterial  films;  (2)  the  prevention  of 
extreme  mobility;  (3)  the  medicinal  treatment  and  the  prophylaxis,  or 
prevention  of  a  relapse  into  the  diseased  condition. 

The  Removal  of  the  Causes. — Calculus  being  an  obvious  irri- 
tant, it  should  be  removed  from  crowns  and  all  parts  of  the  roots.  To 
prevent  infection  of  surrounding  tissues  and  to  remove  the  pus  present 
the  pockets  are  to  be  flushed  out  with  hydrogen  dioxide,  which  may 
be  done  by  means  of  a  sp'inge  with  fine  nozzle  or  an  atomizer  operated 
by  compressed  air.  The  forcible  spray  lifts  away  the  gum  margin 
and  cleanses  the  pockets  mechanically  as  well  as  chemically.  The 
mouth  is  sterilized  at  the  same  time.  If  large  quantities  of  supra- 
gingival  calculus  exist,  it  is  well  to  next  remove  the  gross  deposits  and 
permit  the  patient  to  use  an  astringent,  antiseptic  mouth  wash  for  a 
few  days,  or  the  operation  may  be  proceeded  with. 

Following  this,  cotton  containing  25  per  cent,  pyrozone  or  10  per 
cent,  trichloracetic  acid  is  to  be  packed  into  the  gum  pockets  in  ortler 
to  superficially  constringe  the  gum  tissue,  lessen  the  hemon'hage,  and 
render  more  facile  the  removal  of  the  subgingival  calculi.  The 
latter  is  accomplished  with  scalers  of  any  suitable  form,  working 
either  with  a  push  or  pull  cut  as  best  suits  the  case. 

Fig.  524  illustrates  the  method  of  guarding  against  unnecessarily 
wounding  the  soft  tissues.  If  the  calculi  be  extraonlinarily  inaccessible 
the  pockets  may  be  enlarged  by  packing  for  ten  or  fifteen  minutes  with 
cotton  tampons  saturated  with  the  10  per  cent,  trichloracetic  acid, 
which  also  softens  the  calculi,  or  salicylized  cotton  may  be  left  in  the 
pocket  for  a  day  (Black),  In  some  cases  cocaine  injections  or 
applications  of  powdered  cocaine  carried   into  the  pocket  on   the 


636 


PYORRHEA  ALVEOLARIS 


working  instruments  must  be  made  to  prevent  excessive  pain.  After 
removal  of  the  bulk  of  calculus  with  scalers  any  fine  granules  or  gummy 
collections  may  well  be  rubbed  off  with  Rhein's  approximal  trimmers, 
or  Smith's  pyorrhea  instruments.  After  this  medicinal  applications 
are  made.  (See  later.)  The  scaling  of  each  tooth  is  to  be  completed 
at  one  sitting,  as  repeated  scalings  interfere  with  the  regenerative 
process. 

Fig.  524 


Showing  the  manner  of  holding  an  instrument  for  detaching  calcareous  deposits  when  using 
the  pushing  motion.  Tlie  third  finger  rests  on  the  edges  of  the  teeth,  allowing  freedom  of  the 
hand  to  make  rapid  and  effectual  movements  in  dislodging  the  calculi. 

The  glim  marghis  are  not  to  be  unnecessarily  wounded,  but  very 
redundant  granulations  may  be  cut  away.  In  cases  of  excessive  loss 
of  the  pericementum  of  one  root  it  is  well  to  devitalize  the  pulp,  as,  in 
all  probal)ility,  that  organ  will  have  been  overstimulated  and  will  be 
in  a  degenerative  condition,  and  sometimes  is  actually  infected.  An 
abnormal  response  to  thermal   changes  (ordinary  cold)  may  occur 


.     PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS      637 

(hyperemia  or  inflammation),  or  the  pulp  may  fail  to  respond  to 
extraordinary  cold  (ethyl  chloride),  indicating  degeneration.  It  has 
been  claimed  by  Rhein,  Smith,  and  others  that  if  the  pulp  be  devital- 
ized the  nutrition  received  by  it  will  be  diverted  into  the  pericementum, 
to  the  benefit  of  the  latter.  Clinical  experience  seems  to  confirm  this 
statement.  The  method  also  permits  the  use  of  pins  placed  in  the 
root  canal  as  part  of  an  appliance  fixing  the  teeth  in  position.  W.  A. 
Price  recommends  that  an  exposed  pocket  in  the  bifurcation  be  treated 
by  scraping  and  filling  the  same  with  gutta-percha.  If  tiie  jmiIj)  be 
devitalized,  the  bifurcation  may  be  opened  for  the  purpose  of  success- 
fully placing  the  gutta-percha,  which  is  known  to  be  well  tolerated  by 
the  soft  tissues  (Figs.  525  and  526).     In  case  of  hopeless  involvement 


Fig.  52S 


Fig.  526 


PyoiThea  pocket  in  bifurcation. 


The  same  treated  by  scraping  and  filling  with 
gutta-percha.       (Radiographs  by  Price.) 


of  one  root  of  a  multi-rooted  tooth  the  root  may  be  amputated  if  the 
remaining  roots  will  endure  the  strain  put  upon  them.  The  canals 
of  the  roots  must  have  been  previously  carefully  filled. 

Rhein^  calls  attention  to  the  fact  that  collections  are  apt  to  occur 
about  the  surfaces  left  by  the  amputation,  and  that  postextraetion 
resorption  of  the  alveolar  process  occurs.  To  obviate  this  he  suggests 
the  use  of  a  porcelain  root  to  replace  the  lost  root,  and  about  which  the 
tissues  contract  firmly  and  remain  in  a  healthy  condition.  This  oper- 
ation Rhein  terms  "  heteroplasty  following  the  amputation  of  natural 
roots." 

Briefly  outlined  the  process  is  as  follows: 

1.  Prepare  and  fill  the  root  canals  as  far  as  the  pulp  chamber;  fill 
this  with  temporary  stopping. 

2.  Amputate  the  necrosed  root  by  means  of  a  fissure  drill,  and 
remove. 


'  Dental  Cosmos,  September,  1900,  and  September,  1902. 


638 


PYORRHEA  ALV SOLARIS 


3.  Coat  the  root  with  a  film  of  paraffin  to  allow  for  shrinkage  of 
the  porcelain. 

4.  Take  an  impression  of  one-half  of  the  root  (longitudinally)  by 
embedding  in  plaster;  make  articulating  grooves  and  pour  plaster  for 
an  impression  of  the  other  half;  separate  and  remove  the  root  from 
the  plaster. 

5.  Burnish  matrix  platinum  into  each  half  of  the  impression,  stiffen 
with  porcelain,  and  reburnish.  Complete  one  side  with  porcelain  as  in 
inlay  work,  in  the  other  fuse  a  platinum  box  formed  over  a  square 
platinum  pin  (this  pin  should  be  left  in  the  box  until  the  packing  of 
the  porcelain  about  the  box  is  complete). 

6.  Flatten  the  proximating  sides  of  the  halves;  paint  with  thin,  fresh 
body;  press  together  and  fuse. 

Fig.  527 


Heteroplasty  following  the  amputation  of  natural  roots.     (Rhein.) 

7.  Strip  off  all  platinum  and  dress  off  all  protruding  points,  coat  the 
entire  porcelain  with  a  thin  film  of  body,  place  in  furnace  in  an  upright 
position,  and  heat  almost  but  not  quite  to  a  glaze. 

8.  Wash  out  socket  of  natural  root  with  antiseptics  and  remove 
temporary  stopping  from  the  crown  cavity;  try  porcelain  root  in  place, 
and  if  right  dry  everything;  fill  the  box  with  cement,  return  the  root 
to  place,  and  pass  the  pin  through  crown  cavity  and  into  the  root 
box.     Adjust  root,  leaving  a  slight  space  for  an  amalgam  joint. 

9.  Pack  the  crown  cavity  and  the  joint  with  amalgam,  and  at  a  later 
sitting  finish  the  same  (Fig.  527). 

The  Prevention  of  Excessive  Motion. — The  excessive  move- 
ment of  loosened  teeth  but  increases  the  interstitial  gingivitis  in  the 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS      639 

remaining  tissues.  These  demand  rest.  Any  excessive  occlusion  due 
to  the  swelling  of  pericemental  tissue  may  be  compensated  for  by 
grinding  the  occluding  surfaces.  Such  excessive  occlusion  and  motion 
arc  readily  detected  during  the  act  of  occluding  the  teeth  or  by  means 
of  carbon  paper.  Slightly  loosened  teeth  may  be  temporarily  splinted 
with  ligatures  of  wire  or  floss  silk.  To  prevent  the  slipping  of  these 
toward  the  gum  margin  it  has  been  suggestecP  that  small  buttons  of 
Harvard  or  other  adhesive  zinc  phosphate  be  placed  upon  the  labial 
faces  of  the  teeth  while  under  the  rubber  dam  (Fig.  528).  The  floss 
silk  may  be  saturated  with  a  solution  of  chemically  pure  celluloid  in 
acetone  (155  to  500  gr.")  to  render  it  impermeable  and  more  lasting. 
The  preparation  after  application  is  allowed  to  dry  under  the  dam  to  a 
coagulum  and  then  dismissed  for  twenty-four  hours,  when  it  may  be 
polished.     It  lasts  for  several  months.     For  certain  cases  Dr.  Hugh 

Fig.  528  Fig.  529 


Temporary  splint  of  silk  floss  or  silver  wire 
30-gauge  (one  turn  only  shown).  Buttons 
of  zinc  phosphate.     (Rhein.) 

Mitchell  has  suggested  a  bar  of  iridioplatinum  wire  adapted  to  the 
lingual  surface  of  the  teeth  to  be  splinted,  and  soldered  to  simple 
gold  bands  to  be  attached  with  cement  to  two  of  the  teeth  adjoining 
the  loose  teeth.  The  other  teeth  are  braced  to  the  splint  with  fine 
wire,  gold  or  platinum  being  preferred  for  anterior  teeth. 

Such  a  splint  may  be  quickly  made  and  is  very  effective,  all  slipping 
of  ligatures  being  prevented ;  moreover,  the  wire  may  be  kept  awav 
from  the  necks  of  the  teeth  and  the  gums.  After  a  reasonable  period 
of  immobihty  the  attachment  secured  by  treatment  maybe  tested  (Figs. 
530  and  531),  Very  loose  teeth  which  have  lost  much  of  their  sup- 
porting alveolar  process  must  be  secured  by  permanent  splints.  The 
simplest  of  these  is  a  series  of  rings  soldered  together,  or  its  equivalent, 
sliown  in  Fig.  529.  The  teeth  are  firmly  hgated  at  their  necks  with 
floss  silk.  A  wire  measure  is  taken  of  the  entire  circumference  of  the 
teeth  to  be  included,  allowance  being  duly  made  for  burnishing.     A 

'  Reitz.  »  Kowarska's  paste. 


640 


PYORRHEA   ALVEOLARIS 


piece  of  thin  platinum,  No.  34  gauge  and  one-eighth  inch  wide,  is  cut  to 
measure  and  a  lap  joint  made  and  soldered.  The  ring  is  placed  upon 
the  teeth  and  moulded  to  their  surfaces  and  to  their  interspaces.  The 
thinnest  separating  saw  is  used  to  cut  almost  through  the  splint  on  both 
sides  at  one  interspace.  In  this  groove  a  straight  piece  of  the  platinum 
is  placed  and  the  whole  withdrawn  from  the  teeth  and  the  joints 


Fig.  530 


Fig.  531 


Diagram  showing  labial  view  of  Mitchell's 
splint,  with  two  bands  and  wiring. 


Diagram  showing  view  of  Mitchell's  splint, 
with  two  bands  and  bar. 


soldered.  The  process  is  repeated  at  another  interspace  and  so  on 
until  the  piece  is  complete.  If  the  teeth  are  very  tender,  a  plaster 
impression  of  the  tips  of  the  teeth  may  be  taken  and  the  work  done  on 
a  fusible  metal  model.  _  If  space  be  necessary,  the  teeth  may  be  slightly 
disked  upon  their  proximal  sides.  If  such  spacing  be  not  desirable, 
the  necessary  room  can^isually  be  obtained  at  the  median  inter- 


FiG.  532 


Fig.  533 


Fig.  534 


Five  rings  and  included  artificial 
tooth.     (Evans.) 


Two  rings  and  included  arti- 
ficial tooth.      (Evans.) 


Method  of  making  rings 
as  in  Fig.  523. 


space,  but  one  platinum  septum  is  placed  and  the  piece  is  to  be 

somewhat  stiffened  with  solder  at  the  indentations  representing  the 

inter.spaces. 

t^ Evans'  method  is  readily  comprehended  by  reference  to  Figs.  532, 

533,  and  534. 

These  splints  are  to  be  cemented  with  adhesive  zinc  pho.sphate  so 
manipulated  as  to  set  (luickly,  and  this  is  best  done  with  the  rubber 
dam  in  place.     Quick-setting  Harvard  cement  is  excellent. 

The  foregoing  splints  are  too  conspicuous  for  use  in  some  cases. 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     041 

A  simple  device  introduced  by  Dr.  L.  C.  Bryan^  consists  of  a  j)ure 
gold  band  about  one-eighth  inch  wide,  nicely  bevelled  at  its  edges, 
and  adapted  al)out  the  necks  of  the  lower  incisor  teeth  to  be  sjilinted 
in  somewhat  the  same  manner  that  the  splint  illustrated  in  Fig.  529 
is  adapted.  Particular  attention  is  paid  to  the  interspaces  in  the 
entleavor  to  bring  the  labial  and  lingual  sections  together  at  that  point. 
AVhen  ready  the  piece  is  sprung  off,  the  rubber  dam  is  applied,  zinc 
phosphate  is  placed  within  the  band  and  upon  the  necks  of  the  teeth 
at  all  points,  and  the  band  is  put  in  place  and  burnished.  Before  the 
cement  has  set  gold  wire  is  to  be  passed  around  the  interdental  portions, 
tightly  twisted,  and  the  twisted  end  cut  off  to  within  one-eighth  inch 
of  the  band,  and  the  remainder  bent  back  into  the  indentation  in  the 
band.  Dr.  Bryan  recommended  gold  clamps  in  the  place  of  wire, 
but  these  are  difficult  of  adaptation. 

Such  a  piece  is  to  be  placed  only  on  those  lower  incisors  about 
which  salivary  calculus  promptly  collects,  and  should  be  avoided  in 
the  mouths  of  patients  who  will  not  present  frequently  for  prophylactic 
service.  Confined  to  such  cases  they  do  good  service  and  the  cement 
does  not  readily  wash  away;  indeed,  a  slight  coating  of  calcidus  seems 
to  protect  the  surface  of  it  from  solution.  If  the  calculus  be  kept  from 
the  gimi  margin  this  does  no  harm. 

Several  devices  have  been  offered  which  recjuire  the  devitalization 
of  the  pulps  and  filling  of  the  root  canals  of  the  several  teeth  to  be 
splinted. 

D.  D.  Smith^  suggests  reduction  of  the  lingual  surfaces  of  the  teeth 
and  the  fitting  to  them  of  thin  metal  backings,  which,  after  adaptation 
to  the  teeth,  are  perforated  and  pins  are  thrust  through  for  the  root 
canals.  After  soldering  each  pin  to  its  plate,  readapting  the  latter 
and  stiffening  with  solder,  an  impression  is  taken  and  the  plates  are 
united.  The  whole  piece  is  cemented  to  place  with  the  rubber  dam 
in  position.  Occasionally  the  dam  moves  the  loose  teeth  out  of  position 
and  renders  cementation  difficult.  In  such  cases,  if  likely,  put  the  splint 
in  position  and  pack  temporary  stopping  into  the  free  interspaces  on 
the  labial  side  as  a  temporary  stay.  AYith  this  device  one  or  more 
artificial  teeth  may  be  included  to  replace  lost  incisors  (Fig.  535  to 
538). 

Ames^  suggests  that  in  certain  cases  of  lower  incisors  the  teeth  be 
devitalized  and  amputation  be  performed  at  the  neck  of  each.     Each 

'  International  Dental  Journal,  1899.  2  Dental  Digest,  1902. 

3  Dental  Cosmos,  1903. 
41 


642 


PYORRHEA  ALV SOLARIS 
Fig.   535  Fig.  536 


SiJlint  for  securing  previously  treated  lower 

anterior  teeth.     (Ames,  after  Smith.)  Upper  teeth  prepared  for  splint.     (Ames.) 


Fig.  537 


Splint  for  use  in  the  case  shown  in  Fig.  536. 
Fig.  538 


Same  as  Fig.  536.     Splint  in  position. 
Fig.   540  Fig.   541 


Fig.  539 


Root  with  cap  fitted.      (Ames.) 
Fig.   542 


Tooth  with  Richmond  cap.     (Ames.) 


Splint  for  lower  incisors.     (See  text.) 
(Ames.) 


PYORRHEA   ALV SOLARIS  AS  A  MARGINAL  GINGIVITIS     643 

root  is  then  trimmed  and  fitted  with  a  gold  Richmond  cap  without 
pin  (Fig.  539). 

Each  natural  crown  is  slightly  trimmed  and  fitted  with  a  gold  Rich- 
mond cap  with  a  pin  (Fig.  540).  These  two  caps  are  united  with  wax, 
carried  to  the  mouth,  and  adjusted  in  position  (Fig.  541).  Each  is  then 
carefully  removed,  the  natural  crown  laid  aside  (in  water),  and  the  gold 
sections  invested  and  soldered  together.     The  individual  parts  are 

Fig.  543 


Splint  for  lower  incisors.     (See  text.")     (Ames.) 
Fig.  544 


Splint  .and  double  saddle  bridge  combined.     Front  view.     (Ame.«.) 

readjusted  in  the  mouth,  an  impression  taken,  an  investment  made, 
and  all  soldered  together.  The  natural  crowns  are  then  fastened  in 
their  prepared  sockets  with  cement  and  the  piece  is  cemented  to  place. 
Pins  may  be  placed  in  the  roots  if  desired  (Fig.  542). 

If  desired  the  piece  may  be  further  attached  to  the  adjoining  teeth 
by  means  of  the  lingual  plate  and  pin  (Fig.  543).  The  Ames  device 
would  be  useful  in  cases  in  which  approximal  cervical  caries  exists. 


644 


PYORRHEA  ALVEOLARIS 


It  may  be  stated  that  three  or  four  teeth  fairly  loose  individually 
when  united  together  may,  as  a  whole,  be  quite  firm. 

Ames  further  suggests  that  in  case  the  pericemental  attachment  is 
hopelessly  lost,  such  teeth  may  be  extracted,  the  roots  amputated  and 
prepared  as  for  replantation,  and  then  adjusted  in  the  gold  bridge, 
otherwise  made  as  above  described.  These  roots  are  to  go  in  their 
own  sockets,  and,  being  firmly  fixed  in  position,  the  tissues  settle 
about  them. 

Ames  claims  that  the  extension  bridge  shown  in  Figs.  544,  545,  and 
546  lasted  five  years  and  was  in  as  good  condition  then  as  at  the 
beginning.  Fig.  544  gives  the  anterior  view.  Fig.  545  that  of  the  right 
side,  and  Fig.  546  that  of  the  left  side. 


Fig.  545 


Fig.   546 


Right  side  of  extension  bridge  shown  in 
Fig.  544. 


Left  side  of  extension  bridge  shown  in 
Fig.  544. 


Rhein  offers  the  following:  After  pulp  removal  and  root  filling  a 
transverse  groove  is  cut  in  the  lingual  side  of  the  central  or  loose  teeth 
and  a  half-groove  upon  the  mesiolingual  aspect  of  the  pier  teeth. 
A  staple  is  formed  of  triangular  iridioplatinum  wire  to  fit  into  the 
root  canals  of  the  pier  teeth.  To  this  is  soldered  a  pin  for  each  of 
the  central  teeth.  The  face  of  the  wire  should  approximately  fit  the 
bottom  of  the  groove.  Rhein  suggests  the  following  method  of  attach- 
ment: (1)  Fill  the  root  with  a  paper  point,  place  cement  over  that,  and 
fill  the  cervical  margin  of  the  cavity  and  its  floor  with  gold ;  (2)  drill 
through  the  gold  to  the  paper  point,  remove  it,  and  refit  the  retaining 
appliance;  when  ready  set  with  zinc  phosphate,  avoiding  excess;  (3) 
when  this  is  set  cut  away  to  the  gold  and  complete  the  gold  fillings. 

A  less  elegant  but  still  practical  method  would  be  to  cover  the  pins 
with  a  good,  color-keeping  amalgam  pressed  into  the  excess  of  cement 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     645 


before  it  has  set.  The  margins  are  then  to  be  freed  of  cement  and  the 
operation  completed  with  amalgam,  which  later  should  be  polished. 

Smith's,  Rhein's,  and  Ames'  devices  permit  the  use  of  an  artificial 
tooth  if  necessary.  The  same  may  be  said  for  the  device  which  consists 
of  a  series  of  gold  rings  (Evans'). 

For  the  molars  and  bicuspids  Rhein's  device  is  transferred  to  the 
occlusal  surface  (Fig.  548). 

Short  metal  caps  made  for  the  incisal  tips  of  lower  incisor  teeth 
adjoining  a  space  will  successfully  hold  a  bridge  tooth.  The  device  is, 
however,  rather  conspicuous. 

For  the  molar  and  bicuspid  teeth  it  seems  good  practice  to  adapt 
short  crowns  to  the  partially  trimmed  teeth  and  luiite  these  with 
solder.  A  sort  of  bridge  is  thus  made  which  causes  the  teeth  to  be 
firm  even  if  all  are  originally  loose.  It  is  mainly  this  factor  which 
renders  bridge-work  useful  in  pyorrhea  alveolaris  upon  isolated  teeth. 

The  use  of  united  barrel  crowns  reaching  the  gum  margins  is  at 
times  useful,  but  the  configuration  of  exposed  roots  may  render  this 
impossible  in  some  cases. 


Fig.  547 


Fig.   548 


Permanent  splint  for  cases  of  pyorrhea  alveo- 
laris in  upper  or  lower  incisors.      (Rhein.) 


Permanent  splint  for  cases  of  pyorrhea  alveo- 
laris on  molars  and  bicus|)itls. 


By  the  use  of  pure  gold  crowns,  which  may  be  stifiened  occlusally 
with  solder  to  gain  strength,  better  adaptation  at  cervical  portions  may 
be  obtained  by  hand  burnishing  after  cementation  of  the  piece. 

All  appliances  cemented  to  the  teeth  and  having  a  free  margin  are 
subject  in  some  degree  to  a  solution  of  the  cement.  These  cases  should 
be  seen  fre(|uently  in  any  event  for  prophylactic  purposes,  when  the 
condition  of  the  appliance  may  be  noted. 

Extraction  and  bridge-work  may  be  at  once  resorted  to  in  some  of 
the  aggravated  cases,  though  if  the  appliance  be  mechanically  con- 
structed teeth  which  may  be  extracted  with  the  fingers  may  be  firmly 
held  in  splints  for  years.  While  this  is  a  fact,  good  judgment  may 
demand  the  early  removal  of  such  teeth  before  an  a])pliance  is  con- 
structed. 


646  PYORRHEA  ALV SOLARIS 

If  desired  the  bridge  may  be  made  so  as  to  mount  the  natural  teeth 
after  their  extraction,  by  constructing  sockets  of  gold  for  the  reception 
of  the  necks  of  the  teeth  somewhat  after  the  manner  employed  in  the 
Ames  method.  The  sockets  are  then  soldered  to  each  other  and  to 
the  bridge  piers,  after  which  the  teeth  are  attached. 

These  sockets  are  to  be  made  deep  at  first,  and  it  is  well  to  attach 
the  teeth  with  gutta-percha  in  order  that  the  row  of  sockets  or  a  new 
row  may  be  lowered  to  fit  the  gum  if  desirable.  This  will  require  the 
raising  of  the  teeth  to  the  occlusal  level.  Occasionally  the  use  of 
the  overarch  bar  is  demanded  to  prevent  the  overuse  of  the  teeth 
acting  as  piers  for  bridge-work.  The  lateral  support  of  teeth  by 
plates  is  occasionally  of  use  in  pyorrhea,  but  the  question  requires 
careful  consideration  (see  p.  581).  The  prevention  of  mobility 
in  advanced  cases  may  be  at  times  an  impossibility.  In  such  case 
extraction  and  the  use  of  artificial  teeth  is  probably  better  judgment 
than  the  retention  of  the  teeth  until  extracted  one  by  one. 

The  Medicinal  Treatment  and  Prophylaxis. — ^The  pockets  after  scaling 
should  be  forcibly  syringed  or  sprayed  with  hydrogen  dioxide  to 
sterilize  the  pockets  and  remove  particles  of  calculus,  and  then  cau- 
terized with  either  lactic  acid,  full  strength  (Younger);  trichloracetic 
acid,  25  or  50  per  cent,  strength  (Kirk);  or  sulphuric  acid,  25  per 
cent,  strength  (Truman);  or  deliquesced  zinc  chloride.  If  the  case 
be  of  local  origin  the  application  of  tincture  of  iodine  to  the  gums 
every  other  day  and  the  judicious  use  of  a  well-made  and  hard  brush 
(the  "S.  S.  White  21-3,"  'Trophylactic,"  "Sanitol,"  or  Talbot's  will 
serve)  well  charged  with  an  antiseptic  and  astringent  tooth  powder, 
will  cause  the  gums  to  resorb  to  a  healthy  consistency. 

Dr.  A.  B.  Harrower  has  suggested  the  following  formula  for  a 
powder  which  has  in  his  own  and  my  hands  given  good  results  as 
an  astringent  antiseptic : 

IJ. — Magnesium  carbonate lb.  j 

Cream  of  tartar lb.  is.s 

Red  cinchona  bark §ij 

Calcined  alum 5.i 

Oil  peppermint fov 

Oil  cinnamon foiij 

Oil  ro.se  geranium f 3j. 

All  ingredients  to  be  finely  powdered.     The  oils  are  to  be  added  to  the  magne.sium  before 
thorough  mixing  of  the  powders.     The  whole  i.s  to  be  sifted  through  silk. 

Saccharin  may  be  added  to  the  above  as  a  sweetening  agent.     The  powder  when  wet  is  almost 
neutral,  and  should  do  no  harm  in  it.s  limited  use  as  a  tlierapeutic  agent. 

Truman  advocates  the  use  of  quinine  sulphate,  to  be  packed  in  the 
pockets  as  a  germicide  and  as  inhibitory  of  diapedesis  of  leukocytes. 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     647 

Black  has  recommended  the  use  of  the  1-2-3  mixture,  or  phenol 
camphor,  to  be  put  into  the  })ockets  every  three  days,  and  a  few  drops 
to  be  used  on  the  tooth-brush. 

I^. — Oil  of  cinnamon 1  part 

Carbolic  acid 2  parts 

Oil  of  gaultlicria 3  parts. 

PJ. — Gum  camphor, 

Crystal  carbolic  acid fia      q.  s. 

Mix  in  a  mortar  to  an  oily  fluid. 

Argyrol,  a  compound  of  metallic  silver,  is  less  irritatinf^  tluin  silver 
nitrate,  and  may  be  injected  in  25  to  50  per  cent,  aqueous  solution 
with  marked  benefit.     The  application  may  be  made  twice  a  week. 

Silver  lactate  is  useful  and  also  does  not  discolor. 

Regeneration  in  the  pockets  should  not  be  disturbed,  so  that  unless 
the  pus  flow  be  active  one  should  wait  until  sufficient  time  has  been 
afforded  (about  ten  days)  for  granulations  to  form.  If  pus  be  then 
detected  the  pocket  should  be  again  treated  thoroughly.  Good  results 
are  obtained  from  the  use  of  an  astringent  antiseptic  wash  used  in 
forcible  spray  from  an  atomizer  or  introduced  by  means  of  a  S}Tinge. 
This  should  be  done  daily  by  the  patient.  Stagnant  fluids  in  the 
pockets  are  washed  out  and  replaced  by  the  antiseptic,  thus  inhibiting 
the  bacterial  growth  in  the  pockets  and  the  mouth. 

The  teeth  should  be  cleansed  after  meals  to  prevent  media  for 
infection  lodging  about  the  interstices,  after  which  the  antiseptic  spray 
will  aid  in  destroying  bacteria.  The  gums  should  be  massaged  daily 
by  the  thumb  and  forefinger  of  the  patient.  This  strips  the  collec- 
tions from  about  the  gingival  spaces  and  stimulates  a  healthy  cir- 
culation. Gordon  AVliite  suggests  the  rubbing  of  powdered  sulphur 
upon  the  part  while  massaging.  The  application  of  tincture  of  iodine 
every  other  day  is  a  valuable  aid  in  reducing  the  gingivitis. 

Sulphur  carbolate  of  zinc  in  10  per  cent,  solution  is  valuable  as  a 
stimulant  as  well  as  antiseptic  in  case  of  indolent  healing.^ 

Good  results  from  the  application  of  the  ic-rays  and  high-fre- 
quency currents  have  been  claimed  by  Parker,^  Price,  Guy,  Satterlee, 
Tousey,  and  others. 

The  local  treatment  outlined  must  first  be  given  and  the  .i"-rays  and 
high-frequency  currents  used  as  an  adjunct. 

Tousey  recommends  an  .r-ray  tube  made  of  lead  glass  except  for 
a  single  window  of  ordinary  glass,  through  which  the  rays  pass  in  one 

»  Wliitslar,  Dental  Review,  1907.  '  Dental  Cosmos,  December,  1903. 


648  PYORRHEA   ALVEOLARIS 

direction  only,  and  thus  both  patient  and  operator  are  protected  from 
the  unintentional  action  of  the  rays. 

AppHcations  of  a  minute  or  two  have  beneficial  effect.  The  high- 
frequency  currents  are  appUed  by  small  vacuum  tubes  or  electrodes 
directly  to  the  gums.  They  contain  and  emit  violet  and  ultra-violet 
ravs,  which  not  only  stimulate  the  part  through  the  electricity,  but  also 
produce  ozone  upon  the  gum  surface  and  carry  it  in  and  also  produce 
ozone  in  the  tissue  by  electrolysis.  The  ultra-violet  light  has  also 
some  effect. 

Good  results  have  been  obtained  in  some  cases  by  extraction  and 
replantation,  after  root  preparation  and  sterilization  of  the  tooth  and 
alveolus.  The  alveolus  may  have  to  be  deepened.  An  effort  has 
been  made  by  Goadby  to  utilize  the  opsonic  index  in  the  diagnosis  of 
pyorrhea  alveolaris  and  its  treatment  by  means  of  vaccines  prepared 
from  the  variety  of  germ  found  to  be  the  probable  infection,  but  the 
experiments  have  not  as  yet  brought  this  treatment  to  a  stage  of  per- 
fection sufficient  to  definitely  treat  it  in  this  work;  though  it  may 
be  stated  that  the  effort  is  to  raise  the  opsonic  index,  or  in  other 
words  the  property  of  the  blood  serum  which  assists  or  promotes 
phagocytosis,  so  that  the  infection  may  be  killed  out.  That  is,  the 
resistive  force  of  the  patient  is  raised  (see  page  58.) 

If  the  interstitial  gingivitis  underlying  the  case  be  of  systemic  origin, 
— i.  e.,  due  to  auto-intoxication  from  any  disease,  the  alimentary  canal, 
the  pyorrhea  itself,  or  to  drug  action — these  should  have  attention. 
The  systemic  disease  should,  if  possible,  be  cured  by  correct  medical 
attention.  Pyorrhea  patients  are  of  the  hyperacid  type  (Michaels), 
and  treatment  should  be  directed  toward  elimination  of  waste  prod- 
ucts and  the  reduction  of  hyperacidity  by  the  use  of  alkaline  rem- 
edies. The  bowels  should  be  kept  active  and  the  skin  pores  open. 
Brisk  exercise  in  the  open  air,  if  not  specifically  contra-indicated  by 
organic  disease,  is  valuable  in  both  directions.  Warm  baths  followed 
by  cold  douches  and  vigorous  rubbing  stimulate  the  skin.  Turkish 
baths  followed  by  massage  directed  to  stimulation  of  the  eliminating 
organs  are  valuable  unless  contra-indicated.  Free  drinking  of  pure 
water  is  necessary  to  the  successful  elimination  of  the  waste  prod- 
ucts of  the  body.  The  water  entering  the  blood  increases  the  blood 
pressure  and  flushes  the  tissues  and  the  kidneys,  dissolving  waste 
products.  Water  should  be  freely  taken  between  or  before  meals  in 
order  that  digestion  be  not  interfered  with,  and  if  medicated  with 
salts  of  lithium  the  alkalinizing  effect  and  solvent  action  of  lithium 


SYSTEMIC  EFFECTS  OF  PYORRHEA   ALVEOLARIS  049 

upon  urates  are  obtained.  Patients  exhil)iting  an  aversion  to  water 
drinking  are  more  apt  to  take  it  when  medicated  than  as  a  physio- 
logical necessity.     (See  also  pages  97  and  002.) 

The  prophylaxis  of  pyorrhea  alveolaris  is  all  important,  especially 
in  the  cases  of  systemic  origin  in  which  chronic  disease  or  malnutrition 
may  not  be  readily  overcome  owing  to  confirmed  habit  of  life  or 
advanced  stage  of  disease.  The  local  conditions  existing  even  after 
a  cure  of  pyorrhea  are  such  as  to  invite  reinfection  and  the  establish- 
ment of  microbic  plaques,  which  frequent  cleansing  of  the  teeth  will 
remove.  The  system  of  monthly  or,  if  necessary,  more  frequent 
cleansing  advocated  by  D.  D.  Smith  should  be  practised.  Its  good 
results  are  particularly  manifest  in  this  class  of  cases.  (See  pages 
397  and  618.) 

Recurrence  of  the  condition  is  probable  if  the  oral  prophylaxis  or 
systemic  treatment  be  neglected.  The  simpler  cases  yield  quite  readily ; 
the  advanced  ones,  in  which  much  of  the  alveolar  process  is  lost,  tax 
the  patience  of  operator  and  patient  alike,  and  are  apt  to  end,  sooner 
or  later,  in  loss  of  the  teeth  affected. 

This  fact,  however,  should  not  prevent  the  retention  of  these  teeth 
by  every  means  at  command  during  the  period  for  which  they  may 
be  made  useful.  If,  however,  any  tooth  prove  an  incurable  source  of 
pus  formation  it  should  be  removed,  otherwise  the  remaining  teeth 
are  continuously  infected. 


SYSTEMIC  EFFECTS  OF  PYORRHEA  ALVEOLARIS. 

It  has  been  abundantly  shown  by  Hunter  and  others  that  the  pus 
of  pyorrhea  and  other  intense  oral  sepsis  is  a  source  of  systemic 
infection,  producing  etlects  ranging  from  gastritis  to  actual  septic 
infection.  The  importance  of  this  fact  is  not  to  be  lost  sight  of,  and 
patients  are  to  be  informed  of  the  dangers  of  constant  pus  formation, 
as  well  as  of  the  presence  of  other  forms  of  sepsis  about  the  mouth 
and  teeth. 

R.  1).  Watkins,  M.D.,  has  examined  the  blood  of  pyorrhetic  patients, 
and  has  found  a  mild  condition  of  septic  blood  similar  to  but  less 
than  found  in  })uerperal  fever  and  advanced  carcinoma  and  in  otluT 
infective  conditions.^ 

Goadln'^  reports  the  cure  of  a  case  of  profound  nuiscular  weakness, 

'  Items  of  Interest,  1904.  '  International   Dental  Journal,  July,   1902. 


650  PYORRHEA  ALVEOLARIS 

mental  depression,  and  insomnia  after  unavailing  general  medical 
treatment  for  neurasthenia,  as  following  the  extraction  of  teeth 
affected  by  pyorrhea. 

Hunter  and  Leith^  have  described  cases  of  subacute  and  chronic 
catarrh  of  the  stomach  and  phlegmonous  gastritis  due  to  the  ordinary 
pyogenic  cocci,  such  as  are  found  in  the  mouth,  and  which  the  gastric 
juice  of  the  stomach  of  the  particular  individual  at  least  was  not 
competent  to  kill.  Considering  the  fact  that  an  oral  subacute 
catarrhal  condition  is  established  in  pyorrhea,  the  local  transfer  of 
the  infection  is  not  surprising.  Park^  believes  many  cases  of  appen- 
dicitis to  be  due  to  oral  infection. 

Kirk  adds  to  this  list  pernicious  anemia,  bronchopneumonia, 
malignant  endocarditis,  pyemic  lymphadenitis,  etc.,  as  possibilities 
of  secondary  infection  or  extension  by  natural  contiguous  channels. 

D.  D.  Smith^  claims  to  have  cured  cases  of  confirmed  nervous 
dyspepsia,  nervous  prostration,  and  other  local  and  systemic  conditions 
simply  through  constant  dental  prophylaxis. 


PYORRHEA  ALVEOLARIS  NOT  DEPENDENT  UPON  CALCULUS 

FORMATION. 

Phagedenic  Pericementitis. — By  the  term  phagedenic  pericemen- 
titis Black  has  distinguished  a  form  of  interstitial  gingivitis,  the  chief 
characteristics  of  which  are  the  more  or  less  rapid  destruction  of  a  por- 
tion of  the  pericementum  and  the  resorption  of  the  alveolar  process 
contiguous  to  the  lost  area;  leaving  a  pocket  extending  from  the  gum 
margin  which  may  be  partly  intact  to  a  point  deep  in  the  alveolus,  and 
from  which  much  or  little  pus  may  exude.  The  disease  may  be  con- 
sidered under  the  heading  of  pyorrhea  alveolaris,  beginning  with  a 
marginal  gingivitis,  but  of  aggravated  type  and  especially  virulent 
infection. 

Whatever  its  cause,  the  disease  presents  a  peculiar  rate  and  manner 
of  progress  which  warrant  a  special  description. 

Causes. — ^^Phe  causes  of  this  condition  seem  to  l)e  clearly  infective, 
the  evidence  of  this  being  the  fact  that  it  yields  only  to  operation  for 
removal  of  infected  tissue  or  infective  material,  and  to  the  action  of 
germicides.     Without    doubt    systemic    conditions    favoring    tissue 

'  Transactions  Odontological  Society  of  Great  Britain,  International  Dental  Journal,  1899. 

2  Surgery  by  American  Authors. 

'  Proceedings  Philadelphia  County  Medical  Society,  1903. 


PHAGEDENIC  PERICEMENTITIS  651 

debility  may  act  as  predisposing  causes.  A  proportion  of  the  cases 
begin  with  a  marginal  inflammation  of  acute  form,  sometimes  asso- 
ciated with  calculus  formation  and  sometimes  without  it.  In  several 
cases  observed  some  form  of  traumatism,  such  as  violent  and  per- 
sistent wedging,  blows,  etc.,  or  malocclusion,  has  preceded  the  develop- 
ment of  the  disease.  The  infection  usually  spreads  from  one  tooth  to 
another;  in  other  cases  one  or  two  teeth  may  be  the  only  ones  affected. 

Black  failed  to  find  any  association  of  this  condition  with  gout, 
rheumatism,  or  heredity,  but  considered  the  scrofulous  diathesis  and 
anemia  as  general  predisponents.  He  considers  the  deposition  of 
calculus,  if  present,  as  favoring  the  action  of  the  infecting  fungus,  and 
that  the  latter  is  peculiar  and  of  virulent  type,  though  the  specific 
fungus  was  not  established. 

He  views  it  as  an  oral  fungus  not  subject  to  technical  methods  of 
cultivation  and  study  as  yet  developed  by  bacteriologists.  He  regards 
the  pericemental  glands  as  the  avenues  by  which  infection  travels 
from  the  gingival  space  into  the  deeper  portions  of  the  pericementum. 

Pathology. — The  disease  begins  with  a  marginal  infection  which 
inflames  the  pericemental  margin.  The  infection  advances  toward 
the  apex  of  the  root,  either  slowly  or  rapidly,  and  following  often  but 
one  side  of  the  root.  The  pericementum  is  liquefied,  the  alveolar 
process  disappears  by  resorption,  and  a  distinct  pocket  is  formed. 
The  gum  may  be  partly  resorbed  from  about  the  neck  of  the  tooth, 
but  need  not  be  markedly  destroyed. 

Hyperostosis  of  the  outer  edge  of  the  alveolar  process  may  occur 
(Fig.  518),  or  the  process  may  disappear  at  this  point.  When  the 
inflammation  of  the  pericementum  is  deeply  established  the  tooth 
involved  may  shift  its  position  laterally,  carrying  another  tooth  with 
it,  and  elongate  far  beyond  its  fellows,  sometimes  establishing  mal- 
occlusion, but  sometimes  the  teeth  are  not  in  occlusion  at  all.  Black 
considers  diis  due  to  the  pressure  produced  by  the  swelling  of  tiie 
inflamed  pericementum. 

The  advance  of  the  disease  toward  the  apex  may  be  very  rapid, 
the  pericementum  being  destroyed  even  over  the  apex  of  the  root,  or 
of  one  root,  while  the  attachment  upon  the  other  side  of  the  tooth 
may  hold  it  in  position. 

Black  regards  the  absence  of  decided  mobility  of  the  tooth,  even 
though  shortly  after  the  tooth  may  drop  out,  as  characteristic  of  this 
condition. 

Examination  of  the  area  of  the  root  involved  usually  demonstrates 


652  PYORRHEA  ALV SOLARIS 

either  calculi  or  a  substance  of  viscous  nature  or  both  attached  to 
its  surface.  Pus  may  exude  in  some  quantity  from  the  gum  margin, 
but  it  may  not  be  of  great  amount.  Of  course,  the  pocket  may  afi'ord 
ingress  to  the  ordinary  pyogenic  organisms  of  the  mouth,  which  may 
not  be  the  primary  cause  of  the  disease,  but  merely  implanted  upon  a 
favoring  soil.  The  calculus  present  may  be  a  deposit  from  this  pus 
or  from  the  serum  exuded  by  the  inflamed  tissue. 

The  advance  of  the  case  may  be  very  slov^  and  limited  to  the  teeth 
originally  involved.     The  following  is  an  example: 

Miss  H.,  aged  twenty-five  years,  presented  with  well-established 
pockets,  extending  one-half  inch  toward  the  apex,  upon  the  mesial 
aspect  of  the  root  of  the  right  upper  central  incisor  and  distal  and 
distobuccal  aspect  of  the  right  upper  lateral  incisor.     There  was  a 

Fig.  549 


Phagedenic  pericementitis.  Pockets  as  shown.  Teeth  were  one-sixteenth  inch  longer,  but 
have  been  shortened.  Practically  no  calculus  and  but  slight  flow  of  thick,  creamy  ])us.  Gum 
prominent  over  affected  teeth.     Condition  in  1904. 

history  of  traumatism  due  to  violent  and  persistent  wedging  with 
rubber  at  about  the  age  of  sixteen.  The  case  was  then  of  several 
years'  standing,  and  the  two  teeth  elongated  about  one-eighth  inch 
beyond  their  fellows  (Fig.  549).  The  pockets  were  treated  with 
some  benefit  and  the  teeth  shortened  for  the  cosmetic  effect,  but  the 
{)atient  left  the  city  suddenly  before  recovery,  and  was  not  seen  again 
for  three  years.  At  this  second  visit  it  was  found  that  the  pockets 
were  nearly  the  same  as  at  first  and  no  other  teeth  had  become 
involved.     Nor  had  the  teeth  further  elongated. 

During  the  four  years  from  1904  to  the  present  date  elongation  and 
grinding  have  reduced  nearly  all  the  crown  of  the  lateral,  which  has 
one-quarter  inch  of  its  root  cervix  exposed.  Coincidently  with  the 
exfoliation  the  pockets  have  disappeared  as  though  by  a  drawing  up 


PHAGEDENIC  PElilCEMENTlTlS 


653 


of  the  bottom,  but  the  teeth  are  doomed  and  only  retained  becau.se  of 
the  obstinacy  of  the  patient. 

The  destruction  of  the  tissues  may  assume  several  forn)s.  In  certain 
mouths,  especially  in  neurasthenic  and  anemic  patients,  a  viscous 
material   may   accumulate   upon 

''  ^  Fig.  550 

the  necks  of  teeth  or  exposed 
roots;  and  the  pericementum, 
bone,  and  gum  may  rapidly  in- 
flame and  disappear,  leaving  the 
roots  exposed  to  collect  more  of 
the  material. 
The  resorption  may  occur  as 

shown    in    Fig.    551,   or    the    gum       Destruction  of  pericementum,  bone,  and  gum 

may  be  split  and  the  destruction  ""'"'  '''''''^' '""'  °' "  '"°"^" 

follow  the  length  of  the  root  on  one  side  only  until  even  the  apex  is 
reached  (Fig.  550). 

The  tooth  may  be  loose  or  firmly  attached  by  the  remainder  of  the 
pericementum.  This  is  especially  true  of  those  teeth  having  very 
narrow  necks,  in  which  the  roots  describe  a  prominent  curve  just  above 
the  cervix. 

Fig.  551 


Resorption  of  simi  over  palatal  root  of  an  upper  molar,  as.sociatetl  with  hut  triflinK  deposit  of 
calculus,  but  the  root  is  covered  with  a  viscid  deposit.  Age  thirty-two  years.  Patient  neuras- 
thenic and  of  tuberculous  diathesis.     Condition  in  1904.     Tooth  lost  in  1907. 

Fig.  551  is  a  model  of  the  lingual  side  of  the  right  upper  teeth  untlcr- 
going  the  former  process.  The  left  upper  posterior  teeth  and  the  lower 
incisors  have  also  been  lingually  afi'ected.  There  is  but  little  calculus, 
but  the  viscous  material  is  quite  abundant,  black  stain  is  present,  and 
dental  caries  is  rife.  The  patient  has  been  anemic  and  neurasthenic 
for  years,  and  one  lower  molar  has  been  removed  for  resorption  of  the 
apices  of  the  roots  as.sociated  with  looseness. 

When  pericemental  destruction  has  involved  the  apical  pericenien- 


654  PYORRHEA  ALV SOLARIS 

turn  death  of  the  pulp  occurs,  and  mfection  of  the  necrosed  pulp  results; 
abscess  forms  and  pus  discharges  via  the  pyorrhea  pocket. 

When  the  disease  attacks  but  one  root  of  a  molar,  destruction  of  the 
pericementum  around  that  root,  death  of  half  of  the  pulp,  and  abscess 
formation  may  result,  and  the  other  roots  be  unaffected ;  a  portion  of 
the  pulp  of  the  tooth  may  retain  its  vitality  for  some  time,  notwithstand- 
ing the  apical  abscess  upon  one  root.  In  these  cases  pus  discharge 
from  about  the  root  of  a  tooth  may  be  continued. 

A  form  of  phagedenic  pericementitis  causing  very  rapid  destruction 
of  the  pericementum  and  loss  of  the  teeth  without  loss  of  alveolar  wall 
has  occasionally  been  noted.  In  one  notable  case  two  upper  incisors 
came  away  three  weeks  after  an  ulceration  appeared  about  their  gum 
margins.  The  patient  wore  the  teeth  for  several  weeks  in  situ,  and 
could  remove  and  reinsert  them  at  will.  The  alveolar  walls  were  bare, 
but  intact.  There  was  but  little  pain.  The  sockets  healed  after  re- 
moval of  the  teeth  and  the  freshening  of  the  bone.  While  perhaps 
classifiable  under  this  heading,  the  clinical  features  of  this  case  were 
entirely  distinct  from  those  of  the  phagedenic  condition  recognized  as 
phagedenic  pericementitis,  and  were  more  probably  caused  by  the 
so-called  stomatitis  ulcerosa. 

The  acute  gingival  abscess  sometimes  noted  in  connection  with 
pyorrhea  alveolaris,  and  secondary  to  it,  may  sometimes  occur  in 
connection  with  this  condition  (Figs.  521  and  522). 

While  the  disease  is  usually  first  noted  about  a  single  tooth,  it  is 
rare  that  a  lengthened  period  elapses  before  it  makes  its  appearance 
about  other  teeth ;  usually  an  adjoining  tooth  or,  it  may  be,  on  a  distant 
one.  This  disease  may  make  its  appearance  in  the  mouths  of  patients 
who  take  extraordinary  care  of  the  teeth,  in  mouths  where  the  teeth 
are  apparently  entirely  free  from  deposits,  where  the  gum  appears 
normal,  and  where  the  teeth  are  free  from  caries.  It  is  of  more  fre- 
quent occurrence  in  dentures  comparatively  free  from  caries  than  in 
those  where  caries  prevails  or  has  prevailed. 

Symptoms  and  Diagnosis. — The  disease  being  often  of  rapid  onset, 
nothing  may  be  noted  until  the  patient  complains  of  pain  about  the 
teeth,  when  the  pocket  may  be  found  as  described.  A  line  of  deepened 
color  in  the  gum  over  the  pocket  may  also  be  noted.  The  shifting  of 
teeth  points  to  the  condition;  otherwise  the  signs  noted  under  the 
pathology  are  the  distinguishing  characteristics. 

A  differential  diagnosis  may  have  to  be  made  between  phagedenic 
pericementitis  in  its  later  stages  and  acute  apical  abscess  or  peri- 
cemental abscess. 


PHAGEDENIC  PERICEMENTITIS  655 

Thermal  or  electric  tests,  or  a  history  of  response  to  thermal 
changes,  may  indicate  at  least  partial  vitality  of  the  pulp  which  may 
have  undergone  degeneration.  Any  excessive  response  not  reduced 
by  treatment  of  the  pyorrheal  condition  and  any  lack  of  response 
to  decided  thermal  or  electric  tests  indicate  pulp  inflammation  or 
degeneration  and  a  necessity  for  pulp  devitalization. 

Prognosis. — The  prognosis  of  this  disease,  so  far  as  the  teeth  affected 
are  concerned,  is  in  general  decidedly  unfavorable.  While  it  may  be 
temporarily  arrested  in  its  earlier  stages,  its  recurrence  and  ultimate 
loss  of  the  affected  teeth  are  the  rule.  It  may  attack  but  few  teeth  of 
a  denture  and  progress  until  they  are  lost,  the  other  teeth  remaining 
unaffected.  The  common  history,  however,  is  that  when  the  disease 
makes  its  appearance  the  denture  is  ultimately  lost  through  it,  although 
the  period  of  loss  may  cover  many  years.  Several  years  may  elapse 
between  the  loss  of  one  tooth  and  the  affection  of  the  second.  Upper 
incisors  and  molars  appear  to  suffer  more  frequently  from  the  disease 
than  any  of  the  other  teeth. 

Treatment. — It  has  been  asserted^  that  if  in  the  early  stages — /.  e., 
that  of  tooth  shifting — the  pulp  be  removed  and  the  canal  filled,  the 
impending  degeneration  and  necrosis  of  the  pericementum  will  be 
averted.  The  probable  explanation  is  that  the  diversion  of  the  blood 
stream  of  the  pulp  into  the  pericemental  vessels  enlarges  them  in 
compensation  of  a  degree  of  endarteritis  obliterans  produced  by  the 
interstitial  gingivitis.  Possibly  the  extra  nutrition  thus  obtained  by 
the  pericementum  fortifies  it  against  degenerative  changes,  and 
possibly  even  against  the  existing  infection. 

The  treatment,  as  regards  sphnting  of  the  teeth  and  sterilization  of 
the  pockets,  is  the  same  as  in  the  first  class.  Black  emphasizes  two 
points  of  much  importance  in  the  next  stage  of  treatment — i.  e.,  the 
removal  of  deposits — first,  that  the  gum  margin  must  not  be  unneces- 
sarily injured;  secondly,  that  vigorous  scaling  of  the  roots  may  be  done 
without  special  regard  to  avoid  cutting  the  tissues  lining  the  pocket, 
instead  of  avoiding  such  injury,  as  in  the  first  class  of  pyorrhea.  The 
pockets  are  freely  syringed  with  hydrogen  dioxide,  or  with  a  1  to 
500  solution  of  mercuric  chloride  in  hydrogen  dioxide.  The  alveolar 
edges  are  to  be  freely  scraped  with  the  scaling  instruments,  which 
should  have  slender  stems  and  comparatively  broad  cutting  blades 
(Fig.  552).  The  use  of  cauterants,  such  as  trichloracetic  and  lactic 
acids,  is  more  important  than  in  the  former  type  of  disease.     The  same 

'  M.  L.  Rhein,  D.  D.  Smith. 


656 


PYORRHEA  ALVEOLARIS 


astringent  antiseptic  washes  are  to  be  prescribed.  After  removing  all 
foreign  material,  including  dead  matter,  and  sterilizing,  correcting 
occlusion,  and  securing  immobilty,  the  astringent  antiseptic  wash  is 
expected  to  draw  the  tissues  tightly  about  the  teeth  and  to  prevent 
infection,  so  that  a  regenerative  process  can  be  established  in  the  vital 
tissues  of  the  former  disease  pocket. 

In  case  the  pockets  are  so  deep  or  have  such  form  that  the  alveolar 
margins  cannot  be  well  trimmed  without  overstretching  or  injuring  the 
gingival  edges.  Black  advises  that  gum  flaps  be  raised,  exposing  the 
alveolar  margins  (Fig.  553).  A  semicircular,  incision  is  made  and 
turned  back,  and  bleeding  checked.  By  means  of  sharp  chisels  the 
alveolar  borders  are  freely  scraped,  the  pockets  are  flushed  with 
hydrogen  dioxide,  and  the  flap  secured  by  a  couple  of  stitches.   Cocaine 


Fig.  552 


Fig.  553 


Scalers  (three  times  natural  size). 


Illustration  of  the  position  and  form  of  in- 
cision through  the  gum  for  exposing  the  root 
of  the  tooth  and  injured  alveolar  process:  o, 
incision.     (Black.) 


anesthesia  should  precede  this  operation.  The  same  writer  advises, 
in  cases  where  eversion  of  the  alveolar  margin  has  occurred,  that  the 
process  be  exposed  by  cuts  and  broken  down  by  three  cuts  made  with 
a  sharp  chisel  and  mallet;  the  loosened  segment  of  bone  to  be  pressed 
firmly  against  the  root.  It  is  desired  next  that  the  entire  pocket  will 
fill  with  granulation  tissue,  and  organization  of  the  granulations  take 
place,  furnishing  reattachment.  That  this  occurs  in  some  cases  is 
undoubted.  A  reproduction  of  alveolar  margins  also  occurs  in  some 
cases.  The  hope  of  good  results  lies  in  keeping  the  parts  aseptic 
after  all  foreign  deposits  and  dead  material  have  been  removed. 

For  this  purpose  the  case  should  be  seen  every  few  days  while  under 
treatment,  so  that  the  pockets  may  be  injected  with  antiseptic  sub- 
stances, such  as  1-2-3  mixture  or  phenol  camphor. 

Particular  attention  should  be  paid  to  the  prophylactic  treatment. 


CHAPTER   XXV. 
PERICEMENTAL  ABSCESS. 

In  comparatively  rare  cases  there  begins  in  the  lateral  aspect  of  a 
pericementum  a  swelling  which  finally  discharges  its  contents  either 
at  the  gum  margin  or  directly  through  the  gum  tissue. 

The  pulp  of  the  tooth  may  be  perfectly  vital  and  the  attachment  at 
the  gum  margin  at  first  at  least  practically  unbroken.  A  deposit  of 
calculus  may  or  may  not  be  formed  in  the  area,  and  the  discharge  may 
consist  of  a  glairy  mucus  or  of  purulent  matter.  Cases  of  this 
disease  have  been  noted  and  described  by  Darby  (1874),  W.  E.  Walker 
(1S05),  Tall)ot^  (1S96),  D.  D.  Smith  (1S97),  and  Kirk  (189,S). 

Causes  and  Pathology. — When  seen  as  above  described  the  condition 
occurs  in  the  mouths  of  individuals  predisposed  to  pyorrhea  alveolaris 
associated  with  general  malnutrition^ — i.  e.,  there  is  an  interstitial 
gingivitis  present  in  the  area  affected  that  may  be  predisposed  to  by 
an  auto-intoxication,  the  result  of  a  general  malnutrition  or  intestinal 
toxemia.  The  general  association  of  malnutritional  conditions  with 
an  excess  of  waste  products  in  the  blood  leads  to  the  just  inference 
that  such  waste  floating  through  the  tissues  acts  as  an  irritant,  lessening 
in  time  the  vital  energy  of  the  cells  of  a  part  or  of  the  body  as  a  whole. 
For  this  reason  gout  and  kindred  diseases  are  considered  at  least 
predisposing  causes  of  pericemental  abscess  and  pyorrhea  alveolaris. 

The  frequent  association  of  malnutritional  conditions  with  an  excess 
of  uric  acid  in  the  blood  in  the  form  of  its  urates,  and  the  demon- 
stration by  C.  N.  Peirce,  in  1892,  that  such  urates  exist  in  the 
deposits  upon  the  lateral  aspect  of  the  tooth  aftected,  gave  force  to 
his  claim  that  uric  acid  or  the  waste  products  associated  with  it  are 
responsible  for  the  concretions  and  the  symptoms. 

E.  T.  Darby  (1880),  AV.  J.  Reese  (1886),  and  J.  S.  Marshall  (1891) 
pointed  out  the  relation  of  gout  with  certain  pericemental  conditions. 
Talbot^  has  claimed  that  lead  and  mercurial  poisoning,  scurvy  and 
diabetes  have  lead  to  formation  of  pericemental  abscess. 

1  International  Dental  Journal,  1S9G. 

2  E.  C.  IQrk,  Dental  Cosmos,  November.  1900.  '  Dental  Digest.  1903. 
42 


658  PERICEMENTAL  ABSCESS 

Kirk's  studies  in  pericemental  abscess  have  demonstrated  that  in 
a  few  cases  the  Diplococcus  pneumoniae  may  be  found  in  pure  culture 
in  the  abscess  when  first  opened.  The  question  still  sub  judice  is:  (1) 
whether  the  toxic  waste  products  floating  in  the  sluggish  blood  stream 
of  the  affected  portion  of  the  pericementum  cause  interstitial  gingivitis, 
and  a  necrotic  area  from  which  the  degenerated  tissue  and  coagulated 
lymph  are  expelled  as  the  contents  of  a  pericemental  abscess;  or  (2) 
whether  the  Diplococcus  pneumoniae  or  some  other  organism  enters 
an  area  irritated  by  the  waste  products,  etc.,  and  excites  the  acute 
conditions — such  organisms  have  two  possible  avenues  of  entrance  to 
the  diseased  area :  (a)  via  the  general  circulation ;  (b)  from  the  gingival 
space  via  the  pericemental  glands  of  Black  or  the  bloodvessels;  (3) 
whether  the  said  organisms  are  alone  capable  of  exciting  the  disease 
as  a  purely  local  phenomenon ;  or  (4)  whether  the  associated  calculus 
if  present  is  a  cause  or  result  of  the  gingivitis. 

Talbot  has  claimed  that  pus  contains  much  more  calcium  phos- 
phate than  the  blood,  and  when  present  causes  deposition  of  calculi 
upon  the  roots. 

The  association  of  gout  with  at  least  a  proportion  of  the  cases 
requires  a  consideration  of  its  pathology,  which  will  serve  to  illustrate 
the  principle  of  auto-intoxication.     (See  also  Interstitial  Gingivitis.) 

General  Pathology.  The  conditions  called  gouty  are  held  to  be  due 
to  the  retention  in  the  circulating  fluids  of  an  excess  of  urates,  a  waste 
product  of  tissue  and  food  metabolism;  this  excess  of  material  acts 
as  an  irritant  and  inflammation-exciting  agent  in  the  tissues  of  the 
body,  producing  alterations  of  function  and  structure  in  many  tissues 
and  organs,  but  most  palpably  in  the  members  of  the  connective-tissue 
group.  The  association  of  an  excess  of  urates  with  gout  was  demon- 
strated by  Garrod,  who  detected  crystals  of  urates  in  the  serum  of 
l^listers  from  gouty  patients.  The  association  became  still  more  clear 
after  an  examination  of  the  calculi  of  gout,  which  were  found  to  con- 
tain urates.  In  gouty  joint  affections  urates  of  sodium  are  found 
in  the  diseased  areas,  and  they  constitute  the  common  tophus  found 
in  gouty  patients. 

Urates  of  sodium  are  also  discharged  in  gouty  abscesses  through  the 
skin,  either  in  liquid  or  solid  form,  and  with  or  without  pus  (Musser). 

According  to  Musser^  a  imraber  of  these  abscesses  may  discharge 
without  impairment  of  the  general  health,  or  even  with  benefit  to  the 
system, 

'  Medical  Diagnosis. 


PERICEMENTAL  ABSCESS  659 

It  is  demonstrable  that  the  deposition  of  crystals  of  sodium  l)iurate 
in  and  about  joints  is  the  cause  of  acute  but  non-suppurative  inflam- 
mations of  those  joints.  The  conditions  necessary  for  deposition  seem 
to  be  sluggish  circidation  in  the  part  which  permits  the  urates  to 
infiltrate  into  and  crystallize  in  tissues  somewhat  degenerated  by  the 
sluggish  circulation  and  consequent  deficient  oxidation.  (See  pages 
80  and  94.) 

In  gouty  patients  there  is  a  tendency  to  degenerative  changes,  prob- 
ably induced  in  parts  by  the  irritative  effects  of  the  urates  before 
deposition  in  quantity.  There  is  first  a  tendency  to  sclerosis — i.  c,  to 
the  development  of  the  connective  tissues  at  the  expense  of  the  cellular 
elements  peculiar  to  the  parts. 

Gout,  or  uric-acid  poisoning,  may  exist  as  a  chronic  affection  without 
acute  outbreaks;  deposits  accumulate  in  small  joints  (tophi),  as  of 
the  fingers,  causing  stiffness  and  deformity,  as  the  joints  are  succes- 
sively affected.  An  injury  to  a  joint  may  determine  the  affection  in 
that  joint,  and  any  joint  may  be  affected  (Flint)  (Fig.  52). 

Gout  may  exist  as  an  obscure  affection  without  any  of  the  joint 
affections  noted.  Tophi  may  deposit  in  tendons  (Ziegler).  Disorders 
of  the  stomach,  liver,  kidneys,  heart,  bloodvessels,  and  lungs  may 
all  attend  chronic  gout,  and  be  caused  by  it.  The  evidence  of 
connection  of  obscure  conditions,  such  as  headache,  hebetude  of 
mind,  lassitude;  digestive,  circulatory,  or  respiratory  troubles,  with 
the  gouty  condition,  may  only  be  made  manifest  by  their  relief 
through  antigout  therapeusis. 

All  forms  of  gout  are  largely  hereditary.  The  manifestation  of  the 
diathesis  may  skip  one  generation  and  appear  in  the  next.  Hereditary 
gout  in  the  female  may  manifest  itself  as  rheumatoid  arthritis.  In 
a  proportion  of  cases  no  heredity  can  be  traced,  although  the  existence 
of  gout  in  the  individual  is  unmistakable.  The  deposits  in  gout  are 
only  readily  detectetl  when  they  exist  as  defined  concretions.  They 
may  be  })resent  as  fine  crystals  and  escape  detection.     (See  p.  94.) 

Special  Pathology. — The  test  of  the  soundness  of  the  theory  that 
there  are  distinctive  gouty  dental  affections  depends  upon  whether 
their  causation,  pathology,  and  symptoms  are  ex})lainable  by  the 
phenomena  of  gout  exhibited  in  other  parts,  and,  again,  by  the 
effects  of  antigout  therapeusis. 

First,  an  examination  of  the  teeth  themselves.  Upon  section  the 
enamel,  dentine,  and  cementum  of  the  teeth  lost  by  this  disease  are 
found  to  be  highly  organized.     The  pulp  chambers  are  frequently 


660  PERICEMENTAL  ABSCESS 

almost  obliterated,  even  without  external  evidences  of  abrasion  or 
erosion.  Data  relative  to  the  condition  of  the  pulp  and  pericementum 
are  wanting,  although  from  the  degree  of  immobility  of  the  teeth  it 
may  be  inferred  that  the  pericementum  is  markedly  diminished  in 
volume  prior  to  the  beginning  of  the  disease. 

These  facts  indicate  an  increase  in  the  intercellular  elements  of  the 
parts,  at  the  expense  of  the  essential  cellular  elements  (sclerosis),  as 
a  result  of  a  chronic  irritation. 

The  articulation  of  the  teeth  with  the  maxillse  is  by  implantation  in 
alveoli  (gomphosis),  relation  being  secured  by  the  fibrous  membrane 
— the  pericementum.  While  not  a  joint  in  the  ordinary  sense,  it  may 
be  practically  viewed  as  such.  There  is  no  reason  why  under  certain 
favoring  conditions  urates  may  not  be  deposited  in  the  pericementum 
as  well  as  in  the  metatarsophalangeal  joint  or  in  the  joints  of  the 
fingers  or  the  knee.  That  the  deposit  of  urate  may  be  slight  and 
masked  by  subsequent  deposits  of  calcium  phosphate  does  not  imply 
more  than  that  one  form  of  deposit  is  followed  by  another. 

It  is  probable  that  the  hyperesthesia  about  the  teeth,  accompanied 
by  a  disposition  to  grind  the  teeth  at  night,  and  a  disposition  to  shifting 
of  positions  of  the  teeth  are  explainable  upon  the  ground  of  general 
irritation  of  the  pericementum  as  the  result  of  the  presence  in  them 
of  an  excess  of  urates. 

An  outbreak  of  the  acute  form  of  gouty  pericementitis  upon  some 
one  tooth  is  explainable  by  the  fact  that  an  area  of  debility  has  been 
established  upon  the  said  tooth  by  some  local  cause,  such  as  overuse, 
malocclusion,  disuse,  abuse,  chance  blows,  etc.  The  sluggish  circula- 
tion established  in  the  area  causes  the  deposition  of  urates  to  occur 
in  the  degenerative  tissue  of  the  area.  (See  Calcareous  Degenera- 
tion.) 

Inflammation  of  a  chronic  or  acute  nature  is  excited  and  pyogenic 
infection  may  or  may  not  occur,  either  by  way  of  the  circulation  or 
from  the  gum  margin  by  way  of  the  pericemental  glands  of  Black. 

Teeth  have  been  extracted  during  this  period,  one  of  which  exhibited 
these  signijficant  features:  The  apical  pericementum  was  intact,  as 
was  also  that  portion  toward  the  gingival  margin;  between  the  two 
was  an  area  of  denudation  in  which  loosely  attached  to  the  root  was 
a  rough,  irregular  calculus  (liurchard)   (Fig.  554). 

Calculi  scraped  from  the  roots  of  such  teeth  exhibit  in  a  varying 
degree  a  response  to  the  murexide  test,  the  test  for  urates  (Peirce). 
The  reaction  may  be  very  faint  in  some  cases,  being  overshadowed  by 


PERICEMENTAL  ABSCESS 


661 


the  calcium  phosphate  which  makes  up  the  bulk  of  these  masses;  in 
others  it  is  pronounced — i.  e.,  urates  make  up  a  portion  of  the  deposits. 

Black^  by  test  found  urates  in  nearly  all  concretions,  salivary  and 
serumal,  about  the  teeth.  AVhile  he  claimed  that  this  proved  that 
urates  have  no  causal  relation  to  pyorrhea,  the  findings  seem  rather 
to  point  to  frequent  presence  of  urates  in  the  salivary  and  serumal 
excretions,  which  may  really  be  a  cause  of  irritation  even  when  no 
obvious  symptoms  of  gout  are  present. 

Miller's  demonstration  of  a  calculus  upon  an  unerupted  tooth  is  to 
be  recalled.     (See  p.  624.) 

Other  cases  have  occurred  in  which  no  calculus  was  present,  but  a 
small  sac  was  found  in  the  pericementum,  either  at  the  lateral  aspect 
or  in  the  bifurcation.  This  sac  may  contain  a  globule  of  pus  (1).  1). 
Smith") 


Fig.  554 


Fig.  555 


A  and  C,  vital  pericementum;  B,  gouty  calculus; 
D,  a  subgingival  calculus. 


A ,  calculus  in  area  of  necrosis;   R  and 
C,  vital  pericementum. 


If  a  collection  of  fluid  form  and  discharge  the  condition  is  known 
as  a  gouty  abscess  or,  as  more  lately  termed,  a  pericemental  abscess. 
The  fluid  may  consist  of  coagulated  lymph  or  of  pus.  The  discharge 
in  the  one  case  may  be  glairy,  in  the  other  purulent.  It  is  quite  pos- 
sible, as  shown  by  Talbot,  that  the  pus  may  be  a  cause  of  deposits  of 
calculi  or  that  when  the  organisms  burrow  more  deeply  into  t\\c 
pericementum  from  a  pyorrhea  pocket  a  secondary  pericemental 
abscess  may  result.     (See  p.  633.) 

If  the  abscess  be  located  near  the  gum  margin  it  may  follow  tlic 
pericemental  tract  just  as  an  apical  abscess  may  do  and  discharg(>  at 
the  free  margui.  In  this  case  the  condition  simulates  a  ])yonli('a 
pocket. 


1  Dental  Review,  1S94. 


'  Dental  Cosmos,  1S97. 


662  PERICEMENTAL  ABSCESS 

If  the  abscess  begin  near  the  apex  it  may  find  vent  through  the 
gum  and  thus  produce  a  fistula  simulating  that  of  apical  abscess 
(Fig.  556). 

Morbid  Anatomy. — Aside  from  the  state  of  the  teeth  which  show 
evidences  of  a  tendency  to  secondary  dentine  and  nodule  formation, 
it  has  been  noted  that  the  abscess  is  intrapericemental,  not  sub- 
pericemental.  Figs.  556  and  557  show  the  inflammatory  swelling  of 
the  pericementum,  the  central  abscess  cavity,  and  the  loss  by  resorp- 
tion of  the  alveolar  process  may  easily  be  calculated.  The  original 
chronic  nature  of  the  local  irritation  in  this  case  is  evidenced  by  the 
presence  of  hypercementosis. 

Fig.  556 


Two  views  of  an  intrapericemental  abscess.     Pulp  vital.     (Kirk.) 

In  several  of  these  cases,  where  the  fistulse  have  been  of  long  stand- 
ing, the  editor  has  removed  calculi  (Fig.  555). 

Symptoms. — These  have  been  largely  foreshadowed  in  the  discussion 
of  the  pathology.  Upon  some  vital  tooth  there  appears  an  uneasiness, 
at  first  not  very  painful,  followed  later  by  an  inflammatory  swelling 
which  may  produce  acute  pain  and  then  discharge  a  glairy  fluid  or 
purulent  matter.  There  is  an  absence  of  the  phlegmonous  inflam- 
matory involvement  of  contiguous  tissues  common  in  cases  of  acute 
apical  abscess.  The  fistula  may  persist  after  the  discharge  and  the 
case  may  first  be  seen  in  this  condition. 

D.  D.  Smith  calls  attention  to  the  absence  of  marked  pain  upon 
tapping  and    the  production  of  a  feeling  of  apprehension  upon  the 


PERICEMENTAL  ABSCESS 

Fig.  557 


G63 


Transverse  section  through  buccal  roots  and  pericemental  abscess  shown  in  Fig.  550, 
showing  intrapericemental  abscess  cavity  witli  tistuh)Us  outlet  and  nearby  areas  of  nodular 
hyperceinentosis.      (Kirk.) 


Fig.  558 


Pericemental  abscess.     (Talbot.)     (Photo,  by  Latham.) 


664 


PERICEMENTAL  ABSCESS 


Fig.  559 


part  of  the  patient  during  the  stages  preceding  the  formation  of  the 
fistula.  In  other  cases  the  shifting  of  the  tooth  from  its  position  is 
the  first  noticeable  symptom,  followed  later  by  the  pain,  and  later 
still  by  the  discovery  of  a  pocket  alongside  the  tooth. 

\Miile  the  pericemental  irritation  may  involve  many  teeth,  acute 
outbreaks  are  usually  confined  to  but  one  or  at  most  two  teeth.  The 
disease  subsequently  attacks  other  teeth  singly,  although  these  may 
escape  involvement  for  years. 

Diagnosis. — In  making  the  diagnosis  the  symptoms  described  are 
to  be  borne  in  mind,  but  the  disease  may  be  confounded  with  several 
diseases  having  somewhat  similar  symptoms.  An  acute  apical  abscess 
due  to  gangrenous  pulp  may  be  differentiated 
by  obtaining  evidences  of  pulp  death,  previous 
root-canal  treatment,  etc.  There  is  also  much 
greater  pain  upon  percussion  than  in  perice- 
mental abscess. 

If  the  apical  abscess  be  in  the  third  stage  it 
may  be  differentiated,  if  any  doubt  exist,  by 
incision  and  subsequent  exploration. 

An  acute  lateral  abscess  due  to  a  root  per- 
foration is  more  difficult  of  differential  diag- 
nosis, but  after  incision  evidences  of  perforation 
may  be  sought  externally,  or  the  root  canal  may  be  opened.  In  these 
acute  conditions  the  x-ray  may  render  valuable  aid.  The  pulp 
being  found  alive  by  any  reliable  test  is  evidence  that  the  case  is 
either  one  of  pericemental  abscess  or  of  acute  traumatic  pericementitis. 
In  a  few  cases  of  partial  gangrene  of  the  pulp  the  pulp  may  test  as 
vital,  yet  really  the  symptoms  be  due  to  apical  abscess. 

Acute  traumatic  pericementitis  usually  has  a  history  of  traumatism 
and  presents  more  pain  upon  tapping. 

A  form  of  pericemental  abscess  is  sometimes  found  existing  as  a 
secondary  process  dependent  upon  a  primary  pyorrhea  of  the  first 
class.  The  pus  burrows  from  the  gum  pocket  into  the  gum  tissue  and 
excites  an  abscess  which  discharges  upon  the  lateral  aspect  of  the  gum. 
The  connection  of  the  sinus  at  the  gum  margin  with  the  fistula  will 
demonstrate  their  relation  (Figs.  521  and  522). 

Pericemental  abscess  upon  a  vital  tooth  has  been  seen  associated 
with  a  pyorrhea  pocket,  but  not  directly  connected  with  it.  Probably 
the  infection  has  travelled  via  natural  channels  to  a  deeper  point.  (See 
Fig.  523.) 


A,  calculus. 


PERICEMENTAL  ABSCESS  665 

Again,  a  pericemental  abscess  may  be  caused  by  metastasis  of 
pyogenic  organisms  from  an  acute  apical  abscess — e.  g.,  an  abscess 
in  the  bifurcation  of  the  roots  of  a  molar  may  have  been  caused  by 
bacteria  from  an  apical  abscess;  the  presumption  is  that  the  bacteria 
have  followed  the  pericemental  tract,  perhaps  via  the  glands  of  Black 
or  by  way  of  the  bloodvessels,  and,  finding  a  suitable  location  in  the 
bifurcation,  have  there  developed.  Of  course,  in  such  a  case  the  pulp 
of  the  tooth  in  question,  or  of  that  in  an  adjoining  tooth,  will  be  dead. 
Failing  a  positive  differential  diagnosis,  the  case  should  be  treated 
upon  general  principles — i.e.,  counterirritation,  derivation,  etc.,  and 
decisive  developments  awaited. 

Treatment. — If  the  pericemental  abscess  discharge  by  way  of  the 
gum  margin,  infection  from  the  oral  cavity  occurs  and  the  pocket 
originally  formed  becomes  deeper.  The  case  simulates  then  a  pyorrhea 
alveolaris  beginning  at  the  gum  margin.  The  treatment  is  then  con- 
ducted accordingly.  If  the  swelling  occur  upon  the  gum,  at  a  point 
more  or  less  midway  upon  the  root,  it  shoidd  be  opened  under  anti- 
septic precautions.  An  injection  of  cocaine  solution  should  be  made 
and  a  semicircular  flap  raised.  The  diseased  area  should  be  explored 
for  calculus  and,  whether  found  or  not  found,  the  necrotic  tissue  should 
be  curetted  away.  Next,  the  pocket  should  be  syringed  out  with 
antiseptic.  The  flap  is  next  stitched  into  place  and  the  gum  painted 
over  with  steresol.  (See  p.  267.)  The  mouth  should  be  kept  in  an 
aseptic  condition  during  the  healing  of  the  parts.  AVhether  the  exciting 
cause  of  this  condition  shall  be  finally  shown  to  be  bacterial  or  not, 
the  predisposing  cause  in  a  general  mahiutrition  or  intestinal  toxemia 
should  be  sought  for,  and,  if  possible,  corrected. 

In  the  elimination  of  the  waste  products  which  act  as  irritants  the 
best  results  seem  to  be  attained  by  measures  directed  to  an  increase 
of  the  general  eliminative  functions,  increase  of  tissue  oxidation,  and 
a  restriction  of  diet.  Such  measures  in  general  cause  the  elimination 
of  existing  waste  products  from  the  circulation  and  prevent  the  forma- 
tion of  an  excess  of  new  waste  products.     (See  pages  88, 97,  and  602.) 

Recognizing  the  predisposition  which  exists  in  gouty  persons  to 
active  pericemental  degenerations,  the  operator  should  guard  against 
injuries  to  the  pericementum,  which  might  induce  a  weak  articulation 
and  precipitate  gouty  pericementitis.  Any  malocclusion  should  be 
corrected.  Such  teeth  shoidd  not  be  violently  wedged;  injury  to  the 
gum  or  gum  margins,  by  the  use  of  improper  rubber  dam  clamps, 
ligatures  driven  beneath  margins,  etc.,  may  excite  the  first  stages  of 
a  degeneration  which  will  end  only  in  the  loss  of  the  abused  tooth. 


CHAPTER  XXVI.      ■ 
REFLEX  DISORDERS  OF  DENTAL  ORIGIN. 

Recognizing  pain  as  a  condition  produced  through  the  overexcita- 
tion of  sensory  nerves,  a  reflex  pain  may  be  defined  as  a  pain  referred  to 
some  point  other  than  that  of  its  origin.  Pain  referred  to  the  distribu- 
tion of  a  sensory  nerve  may  be  due  to  overexcitation  of  any  portion  of 
the  nerve  in  its  terminal  distribution,  to  diseases  affecting  any  portion 
of  the  nerve  trunk,  or  to  disorders  affecting  the  central  termination  of 
the  nerve.  Again,  irritation  of  one  sensory  nerve  may  be  referred  to 
some  other  sensory  nerve.  The  condition  is  called  neuralgia.  "When 
muscular  motion  or  glandular  secretion  is  excited  by  irritation  of  sen- 
sory nerves,  the  condition  is  called  a  motor  reflex.  Both  motor  and 
sensory  reflexes  are  also  classed  under  the  heading  of  Reflex  Neuroses. 

As  both  the  upper  and  the  lower  teeth  and  their  surroundings 
receive  their  neural  supply  from  branches  of  the  fifth  pair  of  cranial 
nerves,  discussion  of  this  subject  is  confined  to  causes  operating  within 
the  distribution  of  that  nerve. 

As  such  general  conditions  as  malaria,  syphilis,  and  forms  of  anemia 
operate  to  produce  neuralgia  which  may  be  referred  to  the  teeth,  or  the 
parts  about  them,  only  those  cases  will  be  regarded  as  dental  which 
have  undoubtedly  a  dental  origin,  as  evidenced  by  disappearance  of 
the  neuralgia  following  cure  of  the  exciting  dental  condition.  It  should 
be  noted,  however,  that  vague  and  sometimes  severe  pains  referred 
to  the  teeth  may  entirely  disappear  after  the  cure  of  some  constitu- 
tional disorder.  For  example,  cases  of  periodically  recurring  dental 
pain  have  been  entirely  relieved  through  the  administration  of  quinine 
or  arsenic;  the  pains  were  clearly  of  malarial  origin.  Pain  about  the 
teeth  in  syphilitics  has  disappeared  after  the  administration  of  iodides. 
Pain  referred  to  the  teeth  in  anemic  patients  has  disappeared  after  a 
long  course  of  chalybeates. 

Reflexes  of  dental  origin  are  both  motor  and  sensory,  the  latter  far 
outweighing  the  former  in  importance.  Motor  reflexes  may  be  noted 
in  the  quick  spurt  of  saliva  from  the  ducts  of  the  salivary  glands  upon 
infliction  of  pain  in  the  teeth,  and  by  the  spasmodic  contraction  of  the 
muscles  about  the  mouth  when  the  pulp  of  a  tooth  is  deliberately 


REFLEX  NEURALGIA  FROM  EXPOSED  DENTINE  667 

irritated.     Twitching  of  the  muscles  about  the  face  is  a  common 
accompaniment  of  trigeminal  neuralgia. 

Before  direct  association  of  dental  diseases  with  pains  in  other  parts 
can  be  clearly  demonstrated,  a  review  of  those  conditions  of  the  teeth 
attended  by  pain  must  be  made. 

Dental  pain  arises  in  consequence  of  disorder  of  the  sensory  struc- 
tures; these  are  situated  in  the  pulp,  and  are  continuous  throughout 
the  dentine  and  in  the  pericementum.  Dental  pains,  therefore,  may 
be  discussed,  first,  in  connection  with  affections  of  the  dentine  and 
pulp,  and  secondly,  with  those  of  the  pericementum. 

It  was  stated,  in  discussing  the  diseases  of  the  dental  pulp,  that  this 
organ  is  not  the  seat  of  tactile  sense,  and  that,  like  other  organs 
having  a  kindred  physiological  relationship,  irritation  excited  in  it  is 
not  located,  but  is  referred  to  some  other  part.  While  all  reflex  dental 
disturbances  are,  as  a  rule,  located  in  some  part  of  the  great  nerve 
branch  supplying  the  source  of  irritation,  the  irritation  may  be  reflected 
to  distant  parts;  first,  of  the  same  cranial  nerve,  and  secondly,  to  other- 
nerves.  That  is,  pain  having  its  origin  in  one  of  the  upper  teeth  is 
most  likely  to  be  referred  to  a  point  or  points  in  the  distribution  of  the 
superior  maxillary  nerve.  Disturbances  in  or  about  the  lower  teeth  are 
usually  referred  to  the  distribution  of  the  inferior  maxillary  nerve.  In 
affections  of  either  upper  or  lower  teeth  the  pain  may  be  referred  to  the 
first  division  of  the  fifth  nerve.  In  all  of  these  cases,  but  most  notably 
in  connection  with  disturbances  of  the  upper  teeth,  the  usual  symptom 
of  trifacial  neuralgia — tenderness  of  the  supra-orbital  and  infra-orbital 
nerves  at  their  points  of  emergence  upon  the  face,  the  supra-orbital 
and  infra-orbital  foramina — is  commonly  present. 

Cases  are  extremely  rare  where  the  reflex  pain  is  referred  to  the 
opposite  side;  so  unusual  is  this  occurrence  tliat  its  mention  warrants 
suspicion  that  other  sources  of  irritation  exist  upon  the  side  referred  to. 

The  extent  of  acuteness  of  reflex  pain  bears  no  direct  relation  to  the 
apparent  extent  of  the  source  of  irritation. 

As  might  be  surmised  from  the  function  of  the  dental  pulp,  painful 
reflex  dental  disorders  are  more  common  in  connecticMi  with  (Hsoases 
of  the  pulp  than  with  those  of  the  pericementum. 

REFLEX  NEURALGIA  FROM  EXPOSED  DENTINE. 

The  exposure  of  the  dentine  to  external  sources  of  irritation  is 
followed   by  reactions  governed,  first,  by   the  degree  of  sensitivity 


Fig.  560 


J'laii  of  I  Ik;  fifth  cranial  nerve,  Hhowing  the  reIatioii.slii|>H  of  the  dental  nerves. 
(After  Flower.) 


rV.     f/     REFLEX  NEURALGIA  FROM  EXPOSED  DENTINE  669 

inherent  in  the  protoplasm  of  the  tissue;  and  secondly,  by  the  degree 
of  hypersensitivity  induced  in  it.  Reflex  disturbance  due  to  these 
irritations  is  more  common  in  the  class  of  persons  called  "ncuralgics," 
i.e.,  in  those  whose  nervous  irritability  is  exalted,  a  condition  which 
may  remain  even  in  nervous  exhaustion.  (See  p.  102.)  Like  direct 
pulp  pains,  unless  actual  pressure  be  exerted  upon  the  affected  tissue, 
there  is  no  localized  pain.  In  the  absence  of  deliberate  irritation, 
the  pain  may  be  referred  to  any  portion  of  the  peripheral  distribution 
of  the  fifth  nerve  upon  the  face,  but  if  an  acid  liquid,  such  as  lemon 
juice  or  vinegar,  or  sugars  be  taken  into  the  mouth,  pain  is  excited, 
which  is  referred  indefinitely  to  the  teeth  of  one  side,  frequently  of 
one  jaw.  Reflex  pains  due  to  this  cause  often  appear  when  there 
is  but  little  loss  of  dentine. 

AMien  carious  cavities  have  proceeded  to  any  depth  evidences  of 
direct  pulp  disturbance  are  obtained  through  the  increased  response 
to  thermal  changes. 

Reflex  pains  from  exposed  dentine  aj^pear  most  common  in  con- 
nection with  exposures  at  the  neck  of  the  tooth  and  upon  abraded 
areas.      Obstinate    and  persistent 
neuralgia,    positively    referred    to 
another  nerve  branch,  may  appar-  i 

ently  owe  its  origin  to  so  slight  a  — 37^     , 

cause  as  exposure  at  the  neck  of  a     y^^^      I  g^ 
tooth  of  a  line  of  dentine  (Fig.  5G1).      vT^/ 
The  proof  of   the  connection   be-        Ntigi/ 
tween  the  two  is  made  clear  by  a     '^'^^^  °^  '^*'";'7  '".'^r'T  f'""^."^''*'^  ^^^""- 

■^  atcd  with  reflex  pains. 

disappearance  of  the  neuralgia  after 

the  exposed  dentine  has  been  subjected  to  the  action  of  powerful 
caustics  (especially  silver  nitrate),  destroying  the  dentinal  filaments 
to  some  depth.  Tlie  connection  between  the  two  may  be  revealed 
only  by  accident;  the  contact  of  a  toothpick,  a  dental  instrument, 
or  the  finger-nail  may  induce  a  paroxysm  of  pain. 

^^^lile  in  some  cases  the  dental  origin  of  reflex  pain  may  be  made 
clear  by  the  induction  of  a  painful  response  in  the  area  of  reflection, 
by  irritating  a  tooth  pulp,  this  reaction  is  not  constant.  The  causal 
relation  is  only  certain  when  the  cure  of  localized  dental  disease  is 
followed  by  a  disappearance  of  tlio  neuralgia  without  further  treat- 
ment.    This  jiroof  should  be  exacted  in  all  cases. 

The  most  connnon  sources  of  neuralgic  attacks  about  the  face  are 
diseases  of  the  eyes  and  teeth.     In  general  terms,  diseases  of  the  eye 


670  REFLEX  DISORDERS  OF  DENTAL  ORIGIN 

give  rise  to  reflex  pains  referred  to  the  distribution  of  the  first  branch 
of  the  fifth  nerve;  diseases  of  the  teeth  usually  cause  reflex  pains  in 
either  the  superior  or  inferior  maxillary  divisions,  according  as  the 
upper  or  lower  teeth  are  affected.  In  all  painful  affections  of  these 
nerves  attention  should  at  once  be  directed  to  the  organs  named. 


REFLEX  NEURALGIAS  FROM  PULP  DISEASES. 

The  disturbances  require  classification  according  to  the  distance 
between  their  source  and  their  manifestations. 

In  the  Fifth  Pair  of  Nerves. — ^Pain  referred  to  a  different  spot 
or  ai;ea  than  its  origin  is  a  characteristic  of  all  pulp  diseases.  The 
extent  of  its  reflection  depends,  first,  upon  the  patient,  as  noted  in  con- 
nection with  the  reflex  pains  from  exposed  dentine ;  and  secondly,  upon 
the  variety  of  pulp  disease.  In  neuralgic  patients  any  variety  of  pulp 
disease  may  cause  comparatively  distant  pains.  But,  as  Black  has 
pointed  out,^  the  general  rule  is,  that  the  more  chronic  and  profound 
degenerative  diseases  of  the  pulp  are  much  more  liable  to  give  rise  to 
distant  reflex  pains  than  are  acute  pulp  diseases. 

The  pains  of  acute  hyperemia  and  of  acute  inflammation  of  the 
pulp  are  usually  referred  to  the  region  of  the  tooth  affected,  or  to  a 
corresponding  nerve  trunk.  In  conditions  of  venous  hyperemia, 
nodular  calcifications,  chronic  inflammation,  and,  later,  pulp  degen- 
erations, the  pains  may  be  of  such  character  that  their  dental  origin 
is  only  determined  after  persistent  search.  Particularly  is  this  true 
of  the  growth  of  pulp  nodules.  The  source  of  the  reflex  pains  is  all 
the  more  obscure  from  the  fact  that  in  these  chronic  degenerations 
direct  dental  symptoms  may  be  entirely  absent,  and  are  only  elicited 
upon  the  most  searching  examination  and  exhaustive  tests.  In  some 
cases  of  pulpitis  even  removal  of  the  pulp  by  cocaine  has  been 
followed  by  a  neuralgia  due  to  irritation  of  the  nerve  trunk  in  the 
pulp  stump  at  the  apex,  so  proved  by  cure  through  strong  sedatives 
applied  via  the  canal.     In  one  case  the  neuritis  lasted  several  days. 

There  is  no  constancy  in  the  location  of  the  pain  due  to  any  of 
these  causes;  but  tenderness  of  the  eyeball  upon  pressure;  iritis  or 
conjunctivitis;  persistent  pain  in  the  temporal  and  anterior  auricular 
regions,  particularly  in  connection  with  pulp  diseases  of  the  lower 
posterior  teeth;    in  the  ear  itself,  a  common  site  of  the  reflex  pain 

'  American  Syatem  of  Dcntiatiy,  vol.  i. 


REFLEX  NEURALGIAS  FROM  PULP  DISEASES  671 

excited  by  chronic  pulp  inflammation  and  suppuratioji  of  that  organ; 
behind  the  ear,  back  of  the  lower  border  of  the  mastoid  processes, 
tender  spots  may  develop;  tenderness  to  pressure  may  appear  at  the 
supra-orbital  and  infra-orbital  or  mental  foramen,  and  about  the  ciiin. 
In  the  same  class  of  diseases  the  pains  may  frequently  radiate  as  far 
as  the  shoulder.  Many  of  these  cases 
receive  attention  from  the  general  prac-  ^^^-  ^^^ 

titioner,  and  the  painful  attacks  recur- 
ring at  irregular  intervals  are  relieved 
by  analgesic  remedies — phenacetin,  ace- 
tanilide,  exalgin,  etc. — and  no  attention 
paid  to  a  probable  dental  source  of  the 
disorder.  It  should  be  a  routine  prac- 
tice to  examine  the  teeth  in  cases  pre- 
senting pains  of  the  type  and  in  the 
situations  described.  Acute  diseases  of 
the  pulp,  including  suppuration,  notably 

,  „     ,  ,  11      1  i.  Spots  of  tenderness  in  reflex  neural- 

abscess  ot  the  pulp,  usually  have  atten-  gi^g  ^f  dental  origin. 

tion  directed  to  the  teeth  through  pain 

induced  by  thermal  changes,  so  that  their  diagnosis  is  quickly  made. 
Not  so,  however,  with  the  chronic  degenerative  changes,  except  pos- 
sibly of  pulp  nodules ;  for  if  the  pulp  is  in  the  late  stages  of  degener- 
ation, it  may  require  repeated  applications  of  cold  and  heat  to  elicit 
a  response  from  teeth  which  do  not  respond  by  tenderness  upon 
percussion. 

Failing  to  obtain  evidence  of  pulp  disorders,  examination  should 
be  made  for  exposed  and  hypersentive  dentine.  Then,  examination 
of  the  pericemental  reaction  of  each  tooth  should  be  matle,  and  for 
any  evidences  about  the  teeth  pointing  to  pericemental  disturbance. 
(See  later.) 

Lauder  Brunton*  records  that,  in  his  own  case,  temj)oral  neuralgia 
accompanied  by  tender  eyeball  was  found  due  to  exposed  dentine  uj)on 
the  posterior  cervical  surface  of  a  lower  third  molar  (Fig.  561).  The 
same  writer^  announces  that  "so  frequently  are  headaches  dependent 
upon  decayed  teeth,  that  in  all  cases  of  headache  the  first  thing  I  do 
is  to  carefully  examine  the  teeth;"  as  should  everyone  else.  Brunton 
explains  the  painful  reaction  upon  the  accepted  hypothesis  of  the 
pathology  of  megrim,  that  it  is  due  to  spasmodic  contraction  of  the 

'  St.  Bartholomew's  llosp.  Hep.,  \u\.  xix.      Kei)rinted  in  Iiis  Disorders  of  Digestion. 
2  Ibid. 


672  REFLEX  DISORDERS  OF  DENTAL  ORIGIN 

peripheral  end  of  an  artery,  with  dilatation  of  the  proximal  portion. 
"Irritation  in  the  tooth  is  reflected  to  the  cervical  sympathetic 
ganglia  and  causes  spasmodic  contraction  of  the  arteries  through 
irregular  stimulation  of  the  vasomotor  nerves." 

An  abnormal  tooth  located  in  the  anterior  floor  of  the  nasal  cavity 
was  the  cause  of  headache  for  years,  so  proved  by  cessation  of  head- 
ache after  its  surgical  removal. 


REFLEX  PAINS  FROM  DISEASES  OF  THE  PERICEMENTUM. 

As  a  general  rule,  pericemental  pains  are  located  at  the  affected 
tooth ;  but  in  some  of  the  disorders  the  teeth  may  not  be  tender  upon 
percussion,  and  yet  excite  reflex  pains  in  other  parts,  the  proof  of  the 
connection  being  determined  by  a  disappearance  of  the  pain  upon 
extraction  of  the  tooth.  The  roots  in  such  cases  usually  present 
either  an  hypertrophy  of  cementum  or  show  that  resorption  of  a  por- 
tion— it  may  be  a  major  portion — of  the  root  has  occurred. 

In  cases  of  hypercementosis  it  is  assumed  that  the  source  of  the 
irritation  is  pressure  upon  the  nerves  of  the  pericementum  by  the 
hypertrophic  growth.  Very  widespread  disorders  may  arise  from  this 
source. 

Flagg^  records  many  varieties  of  trifacial  neuralgia;  pains  in  remote 
parts  of  the  body;  grave  functional  disorders  of  the  eye  and  ear;  and 
motor  disturbances — chorea,  epilepsy,  and  paralysis — having  a  direct 
demonstrable  connection  with  hypercementosis.  Insanity  has  also 
been  produced. 

He  mentions  violent  attacks  of  trifacial  neuralgia  as  the  most  com- 
mon reflex  disturbance  from  this  source;  and  next,  long-continued 
pains  in  the  ear  or  eye  of  the  affected  side.  The  existence  of  acute 
disease  of  these  organs  is  usually  diagnosticated  by  the  general 
practitioner.  He  states  that  oral  and  ocular  disturbances,  both 
functional  and  painful,  are  of  gradually  increasing  severity. 

In  examining  for  a  dental  source  of  such  pains,  exposed  dentine, 
pulp  diseases,  and  inflammatory  affections  of  the  pericementum  should 
be  first  excluded.  In  examinations  by  percussion  a  different  response 
may  be  obtained  from  some  one  tooth  than  from  the  others.  Hyper- 
cementosis of  a  particular  tooth  may  be  suspected  by  finding  the  gum 
line  slightly  receded  and  the  tooth  attachment  unusually  firm;  if,  in 

'  Dental  Cosmos,  1878. 


IMPACTED  TEETH  AS  A  CAUSE  OF  NEURALGIA  673 

addition,  vague,  heavy  dental  pains  have  persisted  at  intervals  over  a 
long  period,  the  diagnosis  is  probable.  It  is  only  certain  when  tapping 
upon  the  tooth  brings  on  a  paroxysm  of  neuralgia,  or  where  a  skia- 
graphic  view  actually  exhibits  the  hypertrophic  growth.  The  remedy 
is  extraction.  Any  root  fragment  left  unextracted  may  perpetuate  the 
reflex  disorder.  The  writer  has  recently  treated  a  case  of  neuralgia 
due  to  a  lingual  root  of  a  left  upper  first  bicuspid  which  was  retained 
in  the  gum  after  extraction.  The  gum  had  healed  perfectly  over  it. 
It  Was  only  discovered  by  the  use  of  the  x-rays. 

Painful  afi'ections  referred  to  the  neighboring  region  of  the  afi'ected 
tooth,  or  diffused  through  the  distribution  of  the  corresponding  nerve 
trunk,  or  to  the  eye  or  ear,  may  accompany  the  process  of  resorption 
of  the  roots  of  permanent  teeth.  Gillman^  records  a  case  where  facial 
paralysis  disappeared  upon  extraction  of  a  tooth  which  had  long  been 
the  seat  of  disturbance  and  which,  upon  extraction,  revealed  resorp- 
tion of  its  root.  A  case  of  facial  paralysis  followed  extraction  of 
seven  roots  upon  one  side.  It  was  successfully  treated  by  eight  appli- 
cations of  a  weak  galvanic  current.^  In  these  obscure  cases  the  skia- 
graph, if  taken  at  once,  will  be  a  great  aid  in  the  exclusion  or  diagnosis 
of  pericemental  and  root  abnormalities. 

All  of  the  acute  or  chronic,  septic  or  non-septic,  inflammations  of  the 
pericementum  may  give  rise  to  reflex  pains.  The  most  common 
causes  of  the  reflex  pains  are  found  in  that  stage  of  pericemental  irrita- 
tion which  antedates  acute  septic  apical  pericementitis.  Unless  an 
exacerbation  of  the  reflex  disorder,  or  symptoms  referable  to  that 
region,  be  induced  by  pressure  or  percussion  on  the  tooth,  a  causal 
relationship  is  only  made  out  by  either  relieving  an  existing  dental 
disorder,  an  a;-ray  skiagraph,  or  extracting  the  teeth. 


IMPACTED  TEETH  AS  A  CAUSE  OF  NEURALGIA. 

Neuralgia  of  varying  degrees  of  severity  is  a  common  accompaniment 
of  impacted  teeth.  It  is  most  frequently  noted  in  connection  with  erup- 
tion of  the  lower  third  molars,  not  only  because  this  tooth  is  the  one 
most  frequently  impacted,  but  because  of  the  anatomical  relations  of 
its  roots  with  the  inferior  dental  nerve. 

In  the  milder  forms  of  impaction,  those  in  which  eruption,  though 
delayed,  is  subsequently  completed,  the  pains  are  commonly  localized 

'  Boston  Medical  and  Surgical  Journal,  1S67.  ^  Griefswald,  Cosmos,  1900,  p.  356. 

43 


674  REFLEX  DISORDERS  OF  DENTAL  ORIGIN 

and  associated  with  but  occasional  attacks  of  rigidity  of  the  masseter 
muscles.  If,  however,  the  crown  present  horizontally  or  nearly  so,  and 
its  progress  is  arrested  by  impaction  against  the  posterior  wall  of  the 
lower  molar,  or  if  its  progress  be  arrested  by  permanent  imprisonment 
of  the  advancing  crown  between  the  posterior  surface  of  the  second 
molar  and  the  base  of  the  coronoid  process,  not  only  may  intense  local 
pains  be  induced,  but  severe  reflex  disturbances  of  both  a  sensory  and 
motor  character  may  occur.  In  some  of  these  cases  root  formation  is 
completed,  although  the  crown  of  the  tooth  does  not  advance,  in  which 
case  compression  of  the  inferior  dental  canal  and  its  contents  may 
occur  and  cause  grave  reflex  disturbances.  The  local  irritation  about 
the  root,  due  to  root  growth,  may  excite  continued  constructive  action 
by  the  pericementum,  and  the  h}'pertrophic  growth  in  its  turn  may 
be  the  source  of  reflex  neuralgias. 

Complete  imprisonment  of  the  entire  tooth  has  been  found  to  be  the 
exciting  cause  of  facial  neuralgias,  for  the  cure  of  which  extensive 
surgical  operations  have  been  performed. 

Impacted  cuspids  and  other  teeth  may  excite  no  other  symptoms 
than  reflex  neuralgia.  The  possible  connection  between  an  impacted 
tooth  and  neuralgia  is  made  out  after  excluding  other  dental  causes, 
when  it  may  be  observed  that  one  or  more  of  the  permanent  teeth  are 
absent  from  the  dental  arch,  at  dates  long  after  their  normal  time  of 
eruption. 

A  condition  equivalent  to  partial  impaction,  in  which  dental  irrita- 
tion may  be  the  source  of  reflex  neuralgia,  is  seen  when  the  teeth  are 
crowded — ^jammed  into  arches  too  small  for  their  accommodation. 
During  the  period  of  eruption  severe  maxillary  pains  may  recur  at 
intervals.     The  diagnosis  is  by  means  of  the  x-rays. 


PAIN   REFERRED  TO   NERVOUS  TRACTS    OTHER  THAN 
THE  FIFTH. 

The  most  common  disturbance  appearing  in  other  cerebrospinal 
nerves  than  the  fifth,  due  to  dental  diseases,  is  an  affection  of  the 
eighth  or  auditory  nerve.  Cases  of  deafness  have  been  recorded  due  to 
diseases  of  both  pulp  and  pericementum,  notably  to  hypercementosis. 
Deafness  which  has  persisted  for  a  long  period  has  been  markedly 
lessened  by  the  extraction  of  teeth  the  scat  of  disease.  Cases  of  sup- 
purative otitis  media  have  been  regarded  as  having  pathological  asso- 


PAIN  REFERRED  TO  NERVOUS  TRACTS  675 

ciation  with  septic  diseases  about  the  teeth,  from  the  fact  that  the 
aural  trouble  subsided  immediately  after  extraction  of  the  diseased 
teeth. 

Sensory  disturbances  of  the  eye,  associated  with  dental  diseases,  have 
been  alluded  to;  in  addition  to  these,  grave  structural  and  functional 
diseases  of  the  eye,  traceable  to  dental  causes,  have  been  recorded, 
such  as  motor  and  trophic  disorders/  Among  the  latter  may  be 
mentioned  corneal  inflammation  and  ulceration  and  phlyctenular 
conjunctivitis.  These  are  probably  due  in  part  to  reflex  trophic  dis- 
turbances. 

Irregular  paralyses  of  the  third,  fourth,  and  sixth  nerves  of  the 
affected  side  have  been  noted. 

Amblyopia  and  functional  blindness  without  retinal  conditions  to 
account  for  it  have  been  found  to  arise  from  notably  advanced  degen- 
erative changes  in  the  dental  pulp,  sight  returning  to  the  eye  after 
loss  of  a  diseased  tooth.  DeWitt^  records  a  most  instructive  case 
where  temporary  blindness  was  associated  with  septic  apical  peri- 
cementitis, disappearing  after  evacuation  of  the  abscess  and  reappear- 
ing when  secondary  inflammatory  action  arose  in  the  pericementum. 
The  ocular  affection  disappeared  permanently  and  almost  entirely  with 
the  loss  of  the  tooth.  The  history  of  this  case  illustrates  the  important 
causal  relationship  of  reflex  disturbances  with  late  pulp  degenerations; 
for  the  blindness  arose  two  months  after  some  teeth  were  filled,  and 
existed  for  tw^elve  years  before  the  septic  apical  pericementitis 
appeared. 

A  careful  examination  of  these  and  all  other  reflex  disturbances 
shows  that  pulp  degenerations  outnumber  all  other  affections  as  causes. 
Many  or  most  of  the  cases  are  recorded  by  general  practitioners,  who 
make  no  distinction  between  diseases  of  the  pulp  and  those  of  the  peri- 
cementum, but  a  reliable  diagnosis  of  the  conditions  is  made  possible 
by  the  accompanying  descriptions. 

Cases  of  ovarian  and  uterine  neuralgia  and  sciatica  and  cases  of 
obstinate  pains  in  the  knee,  toes,  and  fingers  have  been  traced  to  dental 
irritation  of  some  one  of  the  varieties  named,  the  proof  of  association 
being  disappearance  of  the  pain  with  loss  of  the  tooth,  though  this  is 
now  not  always  necessary  for  a  cure. 

'  See  Brubaker,  American  System  of  Dentistry,  vol.  iii,  for  very  full  and  detailed  discussion 
of  these  subjects. 

-  Quoted  by  Brunton,  Disorders  of  Digestion. 


676  REFLEX  DISORDERS  OF  DENTAL  ORIGIN 


MOTOR  DISTURBANCES  FROM  DENTAL  DISEASES. 

Motor  disturbances  due  to  dental  irritation  may  occur  as  recurrent 
or  persistent  contraction  or  paralysis  of  muscles,  together  with  more 
or  less  chorea;  in  rare  instances  epilepsy  and  hystero-epilepsy. 
Twitching  of  muscles  of  the  affected  side  of  the  face,  ranging  from 
slight  affection  of  the  occipitofrontalis  or  orbicularis  palpebrarum 
to  recurring  spasm  of  the  elevators  and  depressors  of  the  lower  lip, 
are  far  from  uncommon  phenomena  attendant  upon  pulp  and  perice- 
mental diseases.  In  one  case  mentioned  by  Guilford^  a  pulp  nodule 
was  the  cause  of  tic  douloureux  (painful  muscular  contractions)  of  two 
years'  standing. 

Contraction  of  the  masseter  muscle  is  a  common  accompaniment  of 
retarded  eruption  of  the  lower  third  molar,  which  may  be  intensified 
until  the  condition  is  fitly  termed  trismus,  in  some  cases  of  partial 
impaction  of  the  teeth.  Partial  trismus  has  been  found  due  to  a  general 
overcrowding  of  the  dental  arch.^  Records  of  cases  of  torticollis,  due 
to  dental  diseases,  are  also  given  by  Brubaker. 

Cases  of  facial  paralysis,  and  cases  of  paralysis  of  one  arm,  of  para- 
plegia and  hemiplegia,  and  even  of  general  paralysis,  have  been  noted 
as  disappearing  after  the  extraction  of  diseased  teeth.  It  is  note- 
worthy that  in  these  cases,  as  well  as  in  several  cases  of  tetanus  re- 
corded, the  probability  of  an  infection  entered  into  the  pathogenesis 
of  the  nervous  diseases. 

Stellwagen^  records  a  case  where  symptoms  of  partial  hemiplegia 
followed  upon  the  operation  of  capping  the  pulps  of  two  molar 
teeth;  the  symptoms  disappeared  promptly  upon  extraction  of  these 
teeth. 

Cases  of  insanity  arising  from  dental  diseases  have  been  recorded; 
they  were  both  maniacal  and  melancholic.  In  several  of  them  a 
restoration  to  a  normal  mental  state  followed  promptly  upon  removal 
of  the  offending  teeth.  In  some  of  these  cases  a  preexistijig  maxillary 
neuralgia  directed  attention  to  the  teeth  as  possible  sources  of  the 
nervous  diseases. 

Dr.  E.  Ballard  Lodge^  reports  a  case  from  the  practices  of  Drs. 
Upson  and  Stephan  in  which  a  lady  had  suffered  from  acute  melan- 
cholia   and    insomnia.     A  skiagraph   revealed  an   impacted  upper 

'  I'rivate  communiriaUon.  '  Brubaker. 

3  Private  communication.  ••  Dental  Summary,  1908. 


DENTAL  PAIN  FROM  OTHER  THAN  DENTAL  SOURCES     077 

third  molar  pressing   against   the  distal  side  of  the  seeond  molar. 
Extraction  effected  a  cure. 

Trophic  Disturbances  Following  Dental  Diseases.— ^Two  cases  of 
localized  alopecia  (loss  of  haii')  have  been  reported'  obstinate  during 
the  dental  disease  and  cured  by  the  cure  of  a  pulpitis  in  one  case 
and  extraction  of  a  root  for  suppurative  pericementitis  in  the  other. 
Such  cases  show  a  vasomotor  disturbance  in  the  distant  part. 


DENTAL  PAIN  ARISING  FROM  OTHER  THAN  DENTAL  SOURCES. 

Conditions  of  pain  the  reverse  of  those  discussed — i.  e.,  pain  defi- 
nitely or  indefinitely  located  in  teeth  which  exhibit  no  morbid  con- 
ditions whatever — demand  occasional  attention  at  the  hands  of  the 
dentist. 

Chronic  malarial  poisoning,  as  stated  in  the  beginning  of  this 
chapter,  may  give  rise  to  periodical  attacks  of  maxillary  neuralgia. 
As  in  the  gouty  cases,  the  constitutional  cause  of  the  disturbance  is 
made  clear  through  the  therapeusis  most  effective,  viz.,  the  periodical 
recurrence  of  the  pain  leads  to  the  inference  of  a  malarial  origin,  and 
to  the  administration  of  quinine. 

Syphilitic  pains  in  the  jaws  have  a  pericemental  character,  and  other 
evidences  of  syphilis  are  present  which  point  to  a  diagnosis. 

Pains  in  or  about  the  teeth  are  occasional  accompaniments  of  dis- 
eases of  the  brain  or  its  vessels,  and  of  pregnancy  or  diseases  of  the 
uterus,  kidneys,  and  bladder. 

Disease  in  any  portion  of  the  fifth  cranial  nerve  may  cause  pain 
referred  to  the  teeth. 

Dental  pain  during  pregnancy,  without  any  direct  evidence  of  dental 
disease,  is  relatively  common. 

Disorders  of  the  lower  bowels,  causing  constipation,  may  give  rise 
to  pain  referred  to  one  or  more  teeth,  the  pain  ceasing  promptly  upon 
the  administration  of  an  active  evacuant. 

La  grippe  occasionally  produces  arterial  empyema  or  neuralgia 
about  the  dental  region  as  one  of  its  concomitants  or  sequehe. 

Pain  may  appear  in  one  or  more  teeth  either  with  or  without 
association  with  pain  about  the  maxilla^  or  tenderness  at  foramina  of 
emergence.  If  there  be  possible  causes  in  defective  teeth  or  teeth 
with  fillings  in  which  pulp  irritation  is  a  possibility,  there  may  be  ditti- 

'  Mounier,  Le  Laboratoire,  1907. 


678  REFLEX  DISORDERS  OF  DENTAL  ORIGIN 

culty  of  diagnosis.  There  may  be  a  history  of  an  attack  of  influenza 
or  even  of  coryza,  with  the  common  variety  of  which  dental  pains  are 
often  associated. 

It  may  occur  after  la  grippe  has  seemed  to  have  disappeared.  The 
pain  is  at  first  generalized  over  the  entire  head,  but  gradually 
localized  in  one  or  several  upper  teeth,  more  frequently  in  the  second 
molar,  occasionally  the  bicuspids.  It  sometimes  is  so  severe  that  the 
patient  thinks  an  abscess  is  formmg. 

1'here  is  almost  always  paui  in  the  molar  region  when  pressure  is 
made  upon  the  inner  alveolar  portion  of  the  hard  palate,  and  sensi- 
tivity of  the  external  alveolar  region. 

For  the  pseudoodontalgia  Roy  recommends  a  capsule  containing 
the  following: 

I^. — Antipyrin gr.  vij 

Quinine  hydrobromide gr.  iij 

Sodium  bicarbonate gr.  iij. 

Sig. — One  dose.      Increase  and  prescribe  four  times  a  day. 

Locally  he  recommends : 

I^. — Mentholis gr.  x 

Acidi  borici "  .      oiij 

Vaselini  §j — M. 

Sig. — A  small  portion  to  be  applied  within  tne  nostrils  on  rising  and  retiring. 

Treatment  of  Facial  Neuralgia. — The  cause  should  be  sought  for, 
and,  if  possible,  removed.  If  due  to  diseases  of  the  teeth,  these  should 
be  relieved;  if  due  to  eye  disease,  this  should  receive  attention.  Should 
one  not  discover  the  cause,  yet  desire  to  afford  a  relief  pending  its  dis- 
covery, the  accepted  remedies  antipyrin,  acetanilide,  and  phenacetin, 
combined  with  caffeine  or  the  bromides,  are  useful. 

I^. — Antipyrini  (vel  phenacetini  vel  acetanilidi)       .       .       .       3i 

Caffeine  citratis gr.  x 

Potassii  bromidi 5ii.i — M. 

Ft.  in  chart  No.  x. 

Sig. — One  every  thirty  minutes  until  relieved.      (Hare.) 

If  the  patient  be  constipated,  the  bowel  should  be  freed  of  toxic 
substances  by  the  use  of  castor  oil,  repeated  as  necessary.  Castor  oil 
in  small  doses  is  antineuralgic. 

In  obstinate  neuralgia  and  other  painful  affections  with  unremov- 
able cause,  the  application  of  the  a;-rays  has  been  urged  by  Morton 
as  highly  efficacious  in  relieving  pain  often  for  a  considerable  time. 
The  blue  ray  is  also  used.  A  remedy  of  exceedingly  simple  nature 
was  introduced  by  Verge  and  Pitres  in  1902.  It  consists  of  injecting 
into  the  mucous  membrane  or  skin,  about  where  the  pain  seems  to 


DENTAL  PAIN  FROM  OTHER  THAN  DENTAL  SOURCES     679 

originate,  1  cm.  of  alcohol  at  the  temperature  of  60°  C.  by  means  of  a 
hypodermic  syringe.     Asepsis  must  be  provided  for. 

A  slight  humming  sensation  and  swelling  of  tissue  occurs  about  the 
area  of  injection.  The  pain  disappears  for  a  long  period  after  one 
or  two  injections  a  week  apart. 

A  deep  injection  also  relieves.  A  case  in  which  the  face  became 
black  on  the  side  of  injection  was  also  followed  by  relief  and  subsidence 
of  the  congestion.     The  method  has  been  objected  to  by  some. 


CHAPTER   XXVIL 
INFECTIONS  OF  AND  FROM  THE  MOUTH,  AND  STERILIZATION. 

The  conditions  found  in  the  human  mouth,  as  pointed  out  in 
Chapter  III,  are  of  a  character  which  afford  lodgement  to,  and 
opportunities  for  multipHcation  of,  many  forms  of  bacteria,  both  sapro- 
phytic and  parasitic.  The  oral  conditions  are,  however,  not  entirely 
constant,  so  that  at  different  periods  they  may  favor  the  develop- 
ment of  some  special  bacterial  forms  more  than  others.  The  nature 
of  these  variations  has  not  been  made  out,  although  their  effects  are 
indubitable.  Again,  the  oral  bacterial  inhabitants  are  not  constant 
as  to  species,  for  while  there  are  many  forms  which  appear  to  be 
invariable  occupants  of  the  oral  cavity,  many  pathogenic  forms  are  but 
accidental  residents.  Becoming  resident,  they  may  or  may  not  develop 
according  as  they  find  in  the  mouth  a  suitable  soil.  The  nature  of 
what  constitutes  a  suitable  or  unsuitable  soil  has  not  been  determined, 
although  in  some  cases  extra-oral  culture  experiments  furnish  some 
indications. 

Bacterial  growths,  as  causes  of  dental  caries  and  diseases  of  the 
pulp  and  pericementum,  have  been  discussed  in  connection  with  those 
several  diseases.  It  was  shown  that  the  pyogenic  cocci  are  almost 
constant  inhabitants  of  the  human  mouth.  There  appeared  also 
evidence  that  some  of  the  reflex  disorders  of  distant  parts  are  directly 
traceable  to  septic  processes  about  the  teeth,  and,  in  addition  to  these, 
suppurative  diseases  in  other  parts  become  curable  after  removal  of  a 
septic  tooth,  such  conditions  representing  infection  from  a  local 
dental  infection,  an  important  aspect  of  dental  pathology. 

The  notable  fungus  of  the  blastomycetes  is  the  saccharomyces  albi- 
cans; this  organism,  when  classified  by  mycologists  as  a  thread  fungus, 
was  known  as  the  oidium  albicans  (Fig.  563).  The  growth  of  this 
organism  illustrates  forcibly  the  influence  of  soil  on  the  growth  of 
fungi.  It  does  not  occur  in  the  mouths  of  healthy,  well-nourished, 
and  clean  children  with  good  surroundings.  It  is  a  disease  of  child- 
hood, particularly  of  nurslings,  and  its  occurrence  is  almost  always 
confined  to  bottle-fed  babies  whose  feeding  bottles  are  kept  in  an 


INFECTIVE  BACTERIA  OF  THE  MOUTH 


681 


unclean  condition.  Debility  of  the  oral  tissues  is  established  in  con- 
sequence of  the  fermentations  arisinf^  from  the  source  just  named, 
furnishing  a  favorable  condition  for  the  development  of  the  saccha- 


Fio.  563 


Saccharomyces  albicans,  thrush  fungus. 
(Miller.) 

romyces  (oidium)  albicans.  The  con- 
dition produced  is  known  as  thrush^ 
The  infection  may  be  carried  from  one 
child  to  another,  and  if  the  fungus  be 
brought  in  contact  with  an  abraded 
mucous  surface  of  an  adult  it  may 
develop. 

The  fungus  burrows  between  the 
epithelial  cells  of  the  mucous  mem- 
brane- (Fig.  564),  not  beyond  it.  It 
first  appears  in  small  spots,  which 
coalesce,  until  large  patches  of  a  mem- 
branous-like growth  cover  extensive  surfaces,  spreading  by  con- 
tinuity to  all  of  the  mucous  surfaces  associated  with  the  month. 

As  bud  fungi  flourish  only  in  media  of  acid  reaction,  the  nse  of 
alkaline  washes  is  indicated  in  the  treatment  of  this  condition .  ^^'ipiIlg 
the  patches  with  dilute  phenol-sodique  is  efficacious.  Small  spots 
may  be  cauterized. 

Hydrogen  dioxide  or  25  })er  cent,  iodine  in  glycerin  are  also  nsefnl. 


Pavement  epitlielium  covered  with 
spores  of  (he  oidiuia  albicans.  (Ch. 
Kobin.) 


INFECTIVE  BACTERIA  OF  THE  MOUTH. 


Bacteria,  being  ever  present,  must  always  play  a  part  In  either 
originating,  modifying,  or  associating  with  all  oral  diseases. 


m. 


682  INFECTIONS  OF  AND  FROM  THE  MOUTH 

That  the  progressive  decomposition  of  albuminous  substances, 
always  present  in  the  mouth  to  a  greater  or  less  degree,  by  the  action 
of  saprophytic  fungi,  must  give  rise  to  derivatives  of  albumin,  many 
of  them  toxic  in  effect,  would  be  surmised  even  in  the  absence  of 
experimental  demonstration,  a  suspicion  confirmed  by  experiment. 
Vulpian^  produced  septicemia  by  vaccinating  animals  with  the  saliva 
of  a  healthy  man.  Griffin^  showed  that  the  parotid  saliva  (pure)  is 
harmless.  The  saliva,  if  boiled,  exerts  no  toxic  action,  from  which 
it  is  clear  that  it  derives  its  toxic  substances  from  the  mouth.  The 
saliva  of  individuals  differs  at  times  in  the  degree  of  its  poisonous 
action.     In  some  diseases  it  becomes  intensely  toxic. 

Of  the  many  oral  bacterial  forms,  some  are  cultivable  and  some 
are  not;  hence  the  specific  effects  of  some  are  discovered,  others  are 
doubtful. 

With  regard  to  local  affections,  other  than  those  described  in  the 
body  of  this  book,  a  bacterial  causation  has  been  made  out  in  some, 
but  in  others  it  has  not. 

STOMATITIS. 

Definition. — By  stomatitis  is  meant  a  catarrhal  inflammation  of  the 
mucous  membrane  of  the  mouth. 

Varieties. — It  may  be  localized,  as  in  marginal  gingivitis,  or  be 
diffuse;  and,  again,  be  accompanied  by  localized  tissue  destructions — 
ulcerations;  the  character  of  the  ulceration  differs  according  to  its 
probable  causes. 

Occurrence. — Most  of  these  diseases  belong  to  the  period  of  child- 
hood, although  localized  ulcerative  stomatitis  may  appear  in  the 
adult. 

Causes. — ^The  causes  of  stomatitis  are  so  many  and  varied  as  to 
suggest  a  classification  under  heads  according  to  assignable  causes. 
While  it  is  true  that  bacterial  infection  has  not  been  shown  to  be  a 
direct  cause  of  all  of  these  conditions,  some  degree  of  causal  relation- 
ship is  probable  in  all  of  them.  The  disease  may,  however,  be  included 
under  two  heads  according  as  they  are  or  are  not  localized,  and 
necrotic.  The  less  localized  cases  appear  as  a  dift'use  catarrhal  affec- 
tion, affecting  wide  areas  of  the  oral  mucous  membrane;  the  others 
appear  as  spots  of  localized  tissue  destruction  attended  by  surround- 
ing hyperemia. 

'  Quoted  by  Millftr.  2  Ibid. 


STOMATITIS 


683 


f  Local 


f  Simple. 
(-  Infective 


Catarrhal  stomatitis 


Ulcerative  stomatitis 


Eruptive  fevers. 

Syphilis. 

„  . .        Tuberculosis. 

•- symptomatic  .    „.      ,     .,  , 

>  1  yphoiil  fever. 


Drug  action  . 


Aphthte. 
I  Thrush. 
Local       .       .  •{  Noma. 
Herpes. 
Syphilis  (primary). 


(  Fei 

A  Dii 

'■Go 


Fermentations. 
Diphtheria, 
norrhea. 


(■  Iodides. 
I   Mercury. 
I   Lead. 
|_  I'ilooarpir 


I  /•  g     j^jijg  f  Secondary. 

I  Symptomatic  J     ^P   ' '^  ■       •       •       •  \  Tertiary. 
(.Tuberculosis  (local). 

Simple  Local  Catarrhal  Stomatitis. — The  general  symptoms  of 
catarrhal  inflammation — heat  and  swelling,  with  deepened  color  of 
the  mucous  membrane,  followed  by  increased  secretion  and  exudation 
— attend  several  types  of  oral  irritation,  such  as  the  irritation  induced 
by  erupting  teeth,  particularly  of  the  deciduous  teeth.  Inflammation 
of  any  degree  may  follow  the  taking  into  the  mouth  of  caustic  chemical 
substances,  such  as  caustic  alkalies,  mineral  acids,  carbolic  acid,  etc., 
which  are  occasionally  taken  by  children.  Other  irritant  drugs  and 
very  hot  fluids  may  produce  similar  results.  General  catarrhal  stoma- 
titis is  a  frequent  affection  of  confirmed  smokers,  and  of  drinkers  of 
distilled  liquors. 

The  cure  of  these  conditions  consists  in  the  removal  or  neutralization 
of  the  cause,  and  the  use  of  local  sedatives  and  antiseptics  to  allay 
irritation  and  prevent  infection.  The  most  effective  method  of  treat- 
ing the  inflammatory  condition  is  by  antiseptic  sprays,  such  as  diluted 
Dobell's  solution,  followed  by  sprays  of  strong  solutions  of  potassium 
chlorate.  If  much  pain  exist,  phenol-sodique  is  an  admirable  sedative 
anti.septic,  used  in  10  to  20  per  cent,  solution,  as  a  spray. 

Infective  Local  Catarrhal  Stomatitis. — This  in  some  degree  is  a 
common,  perhaps  the  necessary,  antecedent  condition  to  many  of  the 
ulcerative  forms  of  stomatitis.  It  is  probable  that  many  of  tlie  ca.se.s 
of  stomatitis  found  in  infants,  children,  and  adults  are  due  to  unusual 
fermentations  occurring  in  the  mouth.  Children  whose  nursing  bottles 
are  not  kept  clean;  those  who  at  a  later  age  suffer  from  neglect  of  the 
teeth  and  from  the  eft'ects  of  improper  food ;  adults  in  whose  mouths 
dental  disease  is  widespread,  and  whose  oral  hygiene  is  very  faulty; 
all  exhibit  abnormal  conditions  of  the  oral  mucous  membrane — more 


684  INFECTIONS  OF  AND  FROM  THE  MOUTH 

or  less  swelling,  softness,  and  deepened  color  of  the  mucous  membrane, 
a  coated  tongue,  and  offensive  breath,  with  an  increase  of  oral  secre- 
tions. 

The  complexus  of  oral  symptoms  is  commonly,  and  also  by  the 
general  practitioner,  regarded  as  symptomatic  of  gastric,  intestinal, 
and  hepatic  disorders,  as  doubtless  they  are,  but  the  causal  relationship 
is  in  many  cases  probably  the  reverse  of  that  implied  in  such  opinions, 
for  it  is  probable  that  the  disturbances  of  digestion  are  fermenta- 
tive in  character,  and  the  organisms  causing  them  find  their  way  to 
the  stomach  from  the  mouth,  which  was  first  affected.  The  treat- 
ment of  this  condition  consists  in  the  correction  of  its  causes,  their 
non-repetition,  and  the  continued  use  of  oral  antiseptics. 

^Miile  the  point  of  first  attack  of  the  diphtheria  bacillus  is  most 
marked  about  the  soft  palate  and  tonsils,  the  false  membrane  forming 
there  and  spreading  to  the  pharynx,  more  or  less  general  inflammation 
of  the  oral  mucous  membrane  also  occurs.  The  gonococcus  may  be 
lodged  in  some  portion  of  the  oral  cavity  and  excite  its  specific  effects 
upon  contiguous  mucous  membranes. 

Symptomatic  Catarrhal  Stomatitis. — Stomatitis  in  its  catarrhal 
form  is  usually  associated  with  the  early  and  later  stages  of  the  eruptive 
fevers,  scarlet  fever,  smallpox,  etc.  In  scarlet  fever  and  smallpox 
evidences  of  direct  infection  of  the  mouth  exist  and  the  inflammatory 
reaction  is  pronounced. 

Catarrhal  stomatitis  is  one  of  the  manifestations  of  secondary  and 
tertiary  syphilis,  antedating  the  appearance  of  tissue  necrosis  (ulcera- 
tions). 

More  or  less  catarrhal  stomatitis,  confined,  it  may  be,  to  the  mucous 
membrane  of  the  gums,  is  common  in  the  mouths  of  phthisical  patients; 
this  condition  exhibits  no  evidence  of  direct  association  of  the  local 
development  of  the  bacillus  of  tuberculosis,  because  no  tubercular 
ulcers  may  arise  or  threaten. 

The  stomatitis  of  typhoid  fever  may  be  regarded  as  an  almost 
essential  feature  of  the  disease. 

The  effects  of  drug  elimination  by  the  oral  tissues  have  been  already 
discussed. 

Mercurials  in  excess  produce  gingivitis  with  puffy  gums  which 
bleedLreadily;  there  is  coated  tongue,  fetid  breath  in  marked  cases, 
swollen  tongue  and  cheeks,  and  exfoliation  of  the  teeth.  The  history 
of  administration  of  mercurials,  and,  })ossil)ly,  of  syphilis,  as  a  reason 
for  it  affords  a  diagnosis.     The  mercury  should  be  stopped;  atropine 


STOMATITIS  685 

sulphate,  5  minims  of  a  1-gr.  to  1-oz.  solution  in  \N'ater,  administered 
as  an  antisialagogue  every  four  to  six  hours;  a  5  per  cent,  potassium 
chlorate  solution  in  hydrogen  dioxide  makes  a  useful  mouth  wash  for 
reducing  the  local  inflannnation. 

Ulcerative  Stomatitis. — It  has  been  customary  to  describe  ulcera- 
tive stomatitis  as  simple  and  infective;  in  all  probability  these  ulcera- 
tions are  always  infective.  Like  catarrhal  stomatitis  the  ulcerative 
disease  may  have  only  a  local  significance  or  be  indicative  of  some 
general  disease. 

Ulcerative  Stomatitis  of  Local  Significance. — The  more  usual  or 
infantile  forms  of  these  disorders  are  a  sequel  of  catarrhal  stomatitis, 
at  least  of  an  acquired  debility  of  the  oral  tissues,  and  their  primary 
cause  is,  therefore,  the  cause  producing  a  condition  of  mucous  mem- 
brane which  permits  the  growth  of  infective  organisms.  One  of  these 
diseases,  thrush,  has  already  been  described.  The  others,  aphthae, 
herpes  labialis,  and  noma,  are  all  probably  due  to  the  action  of 
organisms. 

Aphthae. — This  affection  is  common  in  its  isolated  form,  as  the 
canker  sore.  In  the  catarrhal  stomatitis  of  children,  during  or  after 
dentition,  multiple  sores  frequently  make  their  appearance.  The  con- 
dition can  best  be  studied  when  it  appears  as  an  isolated  sore  in  the 
mouth  of  the  adult.  The  most  common  situation  of  the  sore  is  at  the 
junction  of  two  mucous  surfaces,  such  as  that  of  the  gum  with  tlie  lij) 
or  cheek,  or  that  of  the  floor  of  the  mouth  with  the  gum  or  tongue. 
Redness  diffused  over  a  limited  area,  followed  by  a  nodular  hardening, 
occurs,  during  which  local  pain  is  annoying;  the  centre  of  the  hardened 
area  brealis,  the  epithelium  disappearing,  forming  a  raw  surface,  which 
quickly  acquires  a  rough,  yellowish  white  coating  which  is  easily 
removable.     The  sores  are  very  painful. 

The  mouth  is  usually  otherwise  healthy,  and  there  is  an  absence  of 
associated  throat  and  skin  affections. 

This  condition  follows  so  constantly  upon  the  taking  of  very  indi- 
gestible food,  such  as  lobster,  Welsh  rarebits,  etc.,  that  acute  indiges- 
tion must  be  regarded  as  having  some  causal  relationship  with  it.  It 
is  also  of  frequent  occurrence  in  the  mouths  of  dyspeptics;  that  form 
of  gastric  disturbance  attended  by  a  tleficiency  of  hydrochloric  acid  in 
the  gastric  juice  appears  to  have  a  constant  association  with  it,  though 
it  is  probably  caused  by  the  oidium  albicans. 

The  appearance  of  ulcerative  stomatitis  in  children,  together  with 
its  treatment,  was  discussed  in  the  chapter  on  Dentition. 


686  INFECTIONS  OF  AND  FROM  THE  MOUTH 

The  general  treatment  of  these  ulcerations  appearing  in  the  mouths 
of  children  is  the  administration  of  a  laxative,  and  the  subsequent 
administration  of  listerine,  gtt.  x,  every  two  hours.  Locally  the 
mucous  membrane  is  to  be  sprayed  with  pyrozone,  followed  by  sprays 
of  strong  solutions  of  potassium  chlorate. 

Localized  aphthous  patches  in  the  adult  are  promptly  relieved  by 
the  administration  of  calomel,  gr.  ij,  at  night,  followed  in  the  morning 
by  a  mild  saline.  The  local  sore  is  dried  and  touched  with  pure 
carbolic  acid.  The  administration  of  alkalies  before  meals,  and 
hydrochloric  acid  after  meals,  usually  remedies  the  gastric  condition, 
unless  it  be  of  long  standing. 

A  variety  of  aphthous  sore  is  called,  from  the  anatomical  situation 
of  the  ulcers,  follicular  stomatitis.  Irritation  and  swelling  of  the 
mucous  follicles  in  the  palatal,  buccal,  and  labial  mucous  membrane 
are  accompanied  by  more  or  less  localized  inflammation ;  the  follicles 
become  ulcerous,  the  small  ulcers  having  a  uniform  size.  This  con- 
dition quickly  disappears  under  the  treatment  advised  for  ulcerative 
stomatitis.  An  indication  of  the  bacterial  origin  of  all  of  these  dis- 
turbances is  seen  in  the  efficacy  of  antiseptics  used  in  their  treatment. 

Plates  often  cause  ulcerations  and  gingivitis  by  bearing  too  heavily 
upon  certain  parts,  common  localities  being  the  palatomaxillary 
portion  of  the  arch  and  the  labio-alveolar  reflex.  The  plate  should 
be  cut  down  at  such  portions  and  the  part  treated  as  for  aphthae. 


NOMA,  CANCRUM  ORIS,  GANGRENE  OF  THE  MOUTH. 

In  ill-fed,  ill-nourished,  and  ill-kept  cachectic  children,  the  debilita- 
tion of  the  oral  tissues  may  exceed  the  grades  given,  and  a  disease, 
probably  bacterial  in  origin,  may  arise  which  leads  to  widespread 
necrosis  of  the  cheeks  and  maxillae.  The  condition  is  called  gangrene 
of  the  mouth,  noma,  or  cancrum  oris;  the  latter  term  has  been  applied 
to  the  less  severe  varieties. 

This  disease  may  make  its  appearance  as  an  ulcer  at  the  junction 
of  cheek  and  gum;  in  other  cases  a  severe  stomatitis  arises  without  a 
primary  ulcer.  A  greater  or  less  extent  of  the  cheek  acquires  a  board- 
like hardness,  becoming  livid;  the  overlying  mucous  membrane  breaks, 
exhibiting  a  large  slough.  The  necrosis  extends  toward  cheek  and  jaw, 
destroying  further  tissue.  The  sloughs  undergo  putrefactive  decom- 
position, emitting  a  stench.     The  destruction  of  tissue  may  be  arrested, 


NOMA,  CANCRUM  ORIS,  GANGRENE  OF  THE  MOUTH        G,S7 

or  may  proceed,  destroying  in  a  few  days  the  entire  cheek  and  bony 
tissues.  In  the  more  severe  cases  the  disease  is  almost  invariably 
fatal,  because  the  extent  of  the  tissue  destruction  bears  a  constant 
relation  to  the  underlying  debility  of  the  patient.  It  will  be  seen  that 
the  disease  resembles  malignant  pustule  or  carbuncle  in  several  of  its 
features. 

Wliile  no  specific  organism  has  been  isolated  as  pathogenic  of  this 
condition,  Schimmelbosch^  found  a  bacillus  (pure  culture)  upon  the 
borders  of  the  necrosis,  which  may  prove  pathogenic  of  noma. 

Fig.  565 


Noma.      (J.  Lewis  Smith.) 

These  cases  are  purely  medical;  so  that  their  full  discussion  is  not 
warranted  in  these  pages.  The  principle  of  treatment  is  to  inijnove 
the  general  condition  of  the  child,  destroy  the  probable  infection  in  the 
borders  of  the  still  vital  tissue  by  cauterization,  and  promote  sloughing 
of  the  necrosed  tissue  by  the  use  of  antiseptic  applications. 

Dr.  L.  Fisher  (New  York)  reported  a  case  upon  the  inside  of  the 
cheek,  cured  by  applications  of  ichthyol  in  lanolin  four  times  a  day 
over  the  entire  area.^ 


'  .Miller,  Dental  Cosmos,  September,  1891. 
-  Dental  Cosmos,  1902. 


688  INFECTIONS  OF  AND  FROM  THE  MOUTH 

SYPHILITIC    AFFECTIONS    OF   THE   MOUTH. 

The  recognition  of  syphilitic  lesions  about  the  mouth  is  of  vital 
importance  to  the  dental  operator,  first,  because  by  the  recognition 
he  may  take  steps  to  prevent  the  carriage  of  infection  to  innocent 
patients;  and  secondly,  that  he  may  avoid  inoculation  ofjiimself  by 
the  poison. 

In  the  minds  of  many,  syphilis  is  associated  with  the  lower  class  of 
persons,  who  are  confirmed  debauches.  While  it  is  undoubtedly  true 
that  its  prevalence  is  most  marked  in  this  class  of  persons,  it  appears, 
and  with  horrible  frequence,  in  persons  who  would  be  little  suspected 
of  having  such  infection.  The  operator  is  to  be  guided  in  his  opinions 
and  precautions  in  this  matter,  not  by  the  social  status  of  the  patient, 
but  by  the  nature  of  the  morbid  conditions  existing. 

Syphilis  is  usually  divided  into  three  stages,  primary,  secondary,  and 
tertiary;  to  these  may  be  added  a  fourth  stage,  viz.,  in  patients  who 
have  been  discharged  as  cureji  mild  manifestations  of  disorders,  par- 
ticularly of  the  skin  and  mucous  membranes,  make  their  appearance 
from  time  to  time,  and  disappear  promptly  upon  the  administration  of 
iodides.  ^ 

The  first  stage  of  syphilis — ^primary  syphilis — consists  in  the  forma- 
tion of  the  primary  sore  or  chancre,  and  the  involvement  of  the  nearest 
lymphatic  glands.  ^/Secondary  syphilis  is  attended  by  fever,  eruptive 
inflammations  of  the  skin,  inflammation  and  superficial  ulceration  of 
mucous  structures.  ^)ln  tertiary  syphilis  destructive  inflammation  of 
the  skin,  mucous  membranes,  and  connective  tissue  occurs,  together 
with  the  formation  of  specific  tumors — gummata. 

Some  differences  of  opinion  exist  among  syphilographers  as  to  the 
relative  infective  power  of  the  secretions  from  the  several  lesions 
of  syphilis.  All  are  agreed,  however,  that  the  secretions  from  the 
secondary  lesions  observed  in  and  about  the  mouth  are  highly  infective. 
It  is  the  part  of  prudence  to  regard  all  syphilitic  lesions  as  infective. 
All  these  stages  of  syphilis  may  be  seen  in  the  human  mouth.  It  is  to 
be  remembered  that  if  the  mucous  membrane  of  the  mouth  be  infected 
from  a  mucous  patch  (a  secondary  lesion),  the  acquired  disease  will 
appear,  not  as  a  mucous  patch,  but  as  a  chancre.  It  is  from  mucous 
patches  tliat  infection  is  most  to  be  feared. 

Primary  Syphilis  of  the  Mouth. — Causes. — ^llie  primary  lesion 
of  syphilis,  chancre,  when  found  in  the  mouth  is  a  consequence  of 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH  689 

direct  infection  from  a  syphilitic.  The  infection  occurs  from  contact 
of  the  mucous  surface  of  the  mouth  with  a  sj'phihtic  lesion  upon 
another  person :  it  has  been  transmitted  by  kissing;  it  may  occur  from 
using  a  glass  or  cup  previously  used  by  a  syphilitic,  by  smoking  cigars 
or  cigarettes  which  have  been  made  by  syphilitic  cigarmakers,  who 
have  applied  the  tongue  to  the  tobacco  in  attaching  the  wrapper.  Any 
of  the  articles  named,  or  the  contact  of  any  article  which  has  been  in 
contact  with  a  syphilitic  lesion,  if  brought  in  contact  with  an  abraded 
mucous  surface,  may  cause  infection.^ 

The  infection  may  be  transferred  from  patient  to  operator  if  tlie 
fingers  have  any  abraded  surface,  or  if  the  surface  is  broken  accident- 
ally by  an  instrument.  Infection  may  be  transmitted  from  one  patient 
to  another  by  any  instrument,  appliance,  or  article  used  by  a  syphilitic 
being  afterward  used  by  an  hinocent  person.  Drinking  glasses,  mouth 
mirrors,  exploring  instruments,  rubber  dam,  rubber  dam  clamps, 
saliva-ejector  tubes,  lancets,  forceps,  or  any  other  instruments  may 
be  the  medium  of  communication.  During  and  since  the  time  of 
Hunter  the  use  of  teeth  from  syphilitic  patients  in  plantation  opera- 
tions has  been  a  clearly  recognized  medium  of  communication. 
About  32  per  cent,  of  all  primary  chancres  appear  within  the  dental 
field  either  upon  the  lips  or  within  the  mouth.  Dentists  have  been 
inoculated  upon  the  hand. 

Appearances  and  Diagnosis. — "The  primary  lesion  of  syphilis  never 
makes  its  appearance  before  ten  days  after  mfection;  the  maximum 
period  is  about  ninety  days;  the  average  is  twenty-one  days."^ 

It  usually  appears  as  a  single,  elevated,  hard  papule.  In  cases  of 
dental  infection,  most  frequently  about  the  lips,  the  papule  loses  its 
epithelial  coating  after  some  days.  The  induration  surrounding  the 
papular  mass  increases  until  the  papule,  which  is  now  raw  and  in  a 
process  of  ulceration,  appears  surrounded  by  a  ring  of  cartilaginous 
hardness.  This  induration  is  the  one  distii^guishing  feature  of  the 
chancre,  which  is  not  painful.  In  about  a  week  after  the  appearance 
of  the  primary  sore,  swelling  of  the  submaxillary  lymphatic  glands  is 
observed.  In  case  the  chancre  appears  upon  the  tongue,  the  subhy- 
oid lymphatic  glands  are  swollen.^  Unless  pyogenic  nifection  has 
occurred,  the  lymphatic  involvement  is  not  inflammatory,  there  being 

'  Metchnikoff  and  Roux  found  that  an  ointment  composed  of  ten  parts  calomel  and  twenty 
parts  lanolin,  applied  by  inunction  to  an  intentionally  infected  part,  prevented  the  appearance 
of  syphilitic  infection  if  used  within  one  hour  after  inoculation.  Mercuric  chloride  was  of  no 
avail.      Dental  Cosmos,  1907,  p.  1007. 

'  Gross,  System  of  Surgery.  J  Park,  Surgery. 

44 


690 


INFECTIONS  OF  AND  FROM  THE  MOUTH 


no  pain  present.  In  from  three  to  four  weeks  the  sore  disappears, 
leaving  no  signs  of  its  site  in  some  cases;  in  others,  some  induration 
may  persist. 

The  diagnosis  of  this  condition  is  the  important  consideration,  so  far 
as  the  dental  practitioner  is  concerned,  its  treatment  being  the  province 
of  the  general  surgeon. 

The  elevation  of  the  sore,  its  induration,  and,  if  obtainable,  the  time 
of  inoculation,  are  diagnostic  data.  The  sore  is  single,  and  there  is 
hard,  nodular,  painless  swelling  of  the  neighboring  lymphatics.  A 
single  ulcer  of  ulcerative  stomatitis  may  in  some  degree  simulate  the 
appearance  of  a  very  small  chancre.  It  may  exhibit  slight  induration, 
but  its  irregular  form,  situation,  painfulness,  and  the  usual  absence 
of  lymphatic  involvement,  together  with  its  prompt  disappearance 
after  sterilizing  the  mouth  and  cauterizing  the  ulcer,  will  differentiate 
the  two  sores.  If  the  chancre  be  upon  the  tip  or  sides  of  the  tongue, 
where  it  is  subjected  to  irritation,  it  may  become  very  large  and  bear 
a  close  resemblance  to  epithelioma  of  that  organ. 

It  is  a  wise  precaution  to  view  all  sores  about  the  mouth  as  possibly 
infectious.  All  errors  of  diagnosis  in  this  direction  will  be  more  than 
compensated  for  by  the  assurance  of  non-transference  of  infection. 

Secondary  Syphilis  of  the  Mouth. — ^The  secondary  manifestations 
of  syphilis  are  observed  in  and  about  the  mouth,  no  matter  what  the 

location  of  the  primary  lesion 
may  have  been;  they  are  the 
result  of  a  general,  not  a  local, 
infection. 

Secondary  infections  of  the 
mucous  tissues  appear  in  from 
four  to  twelve  weeks  after  the 
appearance  of  the  primary  lesion. 
Sore  throat,  due  to  inflammation 
of  the  mucous  membrane  of  the 
pharynx  and  parts  about,  is 
almost  constant;  together  with 
syphilitic  hoarseness,  due  to  the  extension  of  the  affection  to  the 
mucous  membrane  of  the  larynx. 

The  appearance  of  copper-colored  areas  upon  some  portion  of  the 
mucous  membrane,  on  the  tonsil,  pharynx,  soft  palate,  lips,  or  bucco- 
labial  surface,  precedes  the  loss  of  epithelium  over  these  surfaces, 
which   soon   occurs,  forming  the   most  virulently  contagious   lesion 


Fig.  566 


Chancre  of  the  lip. 


SYPHILITIC  AFFECTIONS  OF   THE  MOUTH  691 

The  patches  become  covered  with 
a  grayish  white,  pasty  covering,  reseinbhng  the  ulcerations  of  non- 
specific stomatitis.  So  close  is  the  resemblance  that  a  differentiation 
can  only  be  made  at  times  by  additional  evidences  of  secondary 
syphilis.  Single  patches  may  coalesce,  forming  large,  irregular 
areas  covered  hy  a  grayish  white  pellicle.  These  patches  are  rarely 
painful.  Ulcerations  having  ragged,  irregular  outlines  may  appear  at 
the  sites  of  the  original  patches  or  in  other  situations,  and  exhibit  a 
tendency  to  spread.  In  healed  cases  the  cicatrices  present  a  whitish 
pellicle  and  contracted  scar,  indicative  of  old  healed  ulcers.  In 
the  skin  little  pits  and  linear  scars  are  symptomatic. 

The  diagnosis  of  the  condition  is  determined  by  a  discovery  of  other 
lesions  of  secondary  syphilis;  skin  eruptions,  falling  out  of  the  hair 
(alopecia),  and  the  areas  of  copper-colored  eruption  upon  the  mucous 
membrane  of  the  pharynx  and  soft  palate. 

Ilugenschmidt^  has  observed  among  syphilitics,  who  presented  no 
local  lesions,  the  frequent  nocturnal  occurrence  of  indefinitely  located 
dental  pains,  spreading  to  the  palatal  region. 

Tertiary  Syphilis  of  the  Mouth.— The  syphilides  of  the  secondary 
stage  arise  in,  and  are  confined  to,  the  mucous  and  dermal  structures; 
those  of  the  tertiary  stage  arise  in  the  deep  connective  tissues,  and 
are  frequently  associated  with  periosteum. 

Tertiary  lesions,  as  seen  by  the  dentist,  are  usually  in  the  form  of 
ulcers  of,  first,  the  soft  or  hard  palate,  and  of  the  tongue  or  lips.  In 
the  earlier  stages  hard,  nodular  formations  may  be  noted  as  ante- 
cedents to  the  ulcerations.  Chronic  periostitis  of  the  palatal  processes 
may  occur,  leading  to  the  formation  of  localized  thickenings.  In  other 
cases,  in  the  soft  palate,  upon  the  tongue,  or  in  the  hard  palate,  local- 
ized swellings  may  occur;  the  overlying  mucous  membrane  breaks, 
establishing  an  ulcer,  which  may  perforate  the  soft  palate  and  destroy 
a  portion  of  the  palatal  process,  or  form  large  ulcers  on  the  tongue. 
The  condition  is  one  of  gumma.  These  lesions  appear  in  from  two 
to  five  years  after  the  secondary  manifestations. 

Although  there  is  much  doubt  as  to  the  degree  of  infectiveness  of 
these  tertiary  lesions,  precautions  as  to  sterilization  should  be  taken  as 
with  the  primary  and  secondary  lesions.  A  defined,  ragged  ulcer 
occupying  the  hard  or  soft  palate,  which  has  persisted  for  a  long  time, 
should  always  be  viewed  with  suspicion,  and  a  search  be  made  for 
other  evidences  of  syphilis. 

'  Dental  Cosmos,  1S92. 


692  INFECTIONS  OF  AND  FROM   THE  MOUTH 

These  ulcerations  appearing  upon  the  side  of  the  tongue  may  closely 
simulate  epithelioma  of  that  organ.  The  confusion  is  increased  if,  in 
consequence  of  the  presence  of  jagged  teeth,  a  continuous  irritation  is 
excited.  Moreover,  leukoplakia  of  the  cheeks,  a  diagnostic  sign  of 
incipient  epithelioma,  frequently  accompanies  tertiary  syphilis.  In 
some  cases  an  absolute  diagnosis  is  only  made  by  noting  the  disappear- 
ance of  the  local  lesion  following  the  administration  of  iodides,  the 
specific  treatment  of  tertiary  syphilis. 

The  existence  of  tertiary  syphilis  is  of  great  clinical  importance  to 
the  dentist  in  that  a  condition  of  lessened  resistance  of  tissues  is  estab- 
lished, and  disease  processes  which  in  the  healthy  person  are  compara- 
tively circumscribed,  in  the  syphilitic  run  a  riotous  course.  A  septic 
pericementitis  by  extension  may  involve  a  wide  area  of  periosteum, 
leading  to  extensive  maxillary  necrosis. 


TUBERCULOSIS  OF  THE  MOUTH. 

The  bacillus  of  tuberculosis,  under  favorable  conditions,  develops  in 
the  tissues  of  the  mouth,  producing  its  characteristic  lesions.  Finding 
a  suitable  soil,  such  as  is  furnished  by  the  heredity  which  predisposes 
to  phthisis  pulmonalis,  the  bacillus  may  find  entrance  to  the  deeper 
tissues  from  the  mucous  membrane  of  the  mouth  and  excite  tuber- 
culosis m  the  deep  structures,  the  bone,  etc.  What  part  is  played  by 
local  oral  and  dental  lesions  in  tuberculosis  of  distant  parts,  by  estab- 
lishing pathways  for  the  entrance  of  the  bacilli  into  the  circulation,  is 
at  present  conjectural,  but  that  such  infections  occur  is  very  probable. 


ACTINOMYCOSIS. 

The  condition  produced  by  the  development  of  the  ray-fungus,  the 
actinomycosis,  in  the  lower  jaw  and  cervical  regions  of  cattle  and 
swine — ^lump-jaw — is  not  unknown  in  human  beings. 

Miller*  gives  203  cases  reported  in  German  medical  literature 
between  1886  and  1891.  In  at  least  120  of  these  cases  the  point  of 
entrance  of  the  fungus  was  found  to  be  in  the  region  of  the  mouth  or 
throat.  Actinomycosis  threads  have  been  repeatedly  found  in  the 
saliva  and  in  carious  teeth,  and  notably  in  the  tonsils.     Whether  the 

'  Dental  Cosmos,  1891. 


GENERAL  SEPTIC  DISEASES  OF  DENTAL  ORIGIN         693 

path  of  entrance  to  deeper  structures  is  ever  through  carious  teeth  is 
undetermined,  but  certainly  lesions  or  wounds  about  the  mouth 
furnish  an  entrance. 

GONORRHEA. 

Undoubted  cases  of  oral  infection  by  the  gonococcus  of  Neisser 
have  occurred.  The  oral  mucous  membrane  and  the  gums  may 
undergo  intense  suppuration.  Fever  and  its  accompaniments  may 
be  present.  The  mouth  and  eyes  are  very  subject  to  secondary  infec- 
tion in  an  individual  suffering  from  gonorrheal  urethritis.  The 
toxins  and  the  germs  formed  in  the  mouth  may  be  swallowed. 


GENERAL  SEPTIC  DISEASES  OF  DENTAL  ORIGIN. 

The  effect  of  the  existence  of  dental  diseases  upon  the  body  at  large, 
particularly  as  regards  secondary  infection,  is  a  matter  increasing  in 
importance  as  the  possibilities  of  their  connection  are  made  out.  At 
present  the  organisms  of  greatest  demonstrable  pathological  interest 
are  the  pyogenic  cocci.  The  almost  constant  presence  of  these 
organisms  in  the  mouth,  carried  thence  into  the  pharynx,  posterior 
nares,  larynx,  lungs,  and  stomach,  furnishes  the  reason  for  the  pyogenic 
and  phlegmonous  inflammations  which  occur  in  these  organs.  The 
diplococcus  of  pneumonia,  a  frequent  organism,  but  waits  a  favorable 
opportunity  to  establish  high  inflammations  and  fibrinous  exudations 
in  the  lungs,  and  possibly  in  other  structures. 

'  The  most  important  clinical  associations  of  dental  with  general 
infections  are  diseases  of  the  pericementum.  The  pulps  of  teeth, 
having  no  lymphatics,  do  not  appear  to  take  up  and  transmit  tiie 
products  of  the  action  of  septic  organisms;  but  while  the  evidences 
of  such  absorption,  involvement  of  the  neighboring  lymphatics,  are 
not  present,  it  must  be  remembered  that  the  veins  may  transmit  the 
poison,  and,  in  addition,  may  perhaps  convey  organisms  from  a 
diseased  but  still  vital  pulp  to  distant  parts.  When,  however,  the 
pulp  is  dead  and  the  pericementum  is  invaded,  there  is  no  doubt  of 
general  infection  from  this  local  source.  More  or  less  septic  intoxica- 
tion is  a  common  attendant  upon  severe  septic  apical  pericementitis 
and  septicemia  accompanied  by  inflammation  of  the  neighboring 
lymphatic  glands  is  of  sufficient  frequency  to  emphasize  the  need  of 


694  INFECTIONS  OF  AND  FROM  THE  MOUTH 

the  vigorous  antiseptic  treatment  recommended  in  all  of  these 
cases. 

Pyemia  is  far  more  uncommon.^  Pyogenic  organisms,  gainmg 
access  to  the  blood  current  from  the  local  source  of  mfection,  establish 
suppuration  in  distant  parts;  in  other  parts  of  the  bone,  or  in  other 
bones  (osteomyelitis),  in  the  lungs,  meninges,  and  substance  of  the 
brain.  One  case^  has  been  reported  where  abscess  of  a  toe,  ear,  and 
forearm  ceased,  and  recovery  took  place  after  treatment  and  filling  of 
septic  root  canals.  Several  cases  are  tabulated  by  the  same  author 
in  which  extensive  necrosis  and  death  resulted  from  pyemic  infection 
from  septic  pericementitis.  Some  of  these  cases  recorded  were  asso- 
ciated with  acute,  some  with  chronic,  septic  pericementitis. 

In  addition  to  the  usual  pyogenic  cocci,  Miller  has  isolated  several 
forms  of  cocci,  baccilli,  and  spirilla,  forming  products  which,  if  injected 
into  the  circulation  of  animals,  cause  death  from  septicemia  in  from 
hours  to  days.  As  many  of  these  forms  may  be  brought  into  relation 
"With  deep  parts  by  the  anatomical  conditions  created  by  pulp  death, 
the  possibilities  of  many  types  of  infection  via  pulpless  teeth  are 
evident. 

The  possibilities  of  local  as  well  as  general  infections  through  the 
conditions  established  in  the  several  forms  of  pyorrhea  alveolaris 
should  not  be  forgotten. 

The  pockets  formed  by  the  soft  tissues  overhanging  lower  third 
molars  whose  eruption  is  impeded  invite  the  passage  of  septic  organ- 
isms to  deep  parts.  Local  pyogenic  infections  are  common  in  these 
cases. 

HERPES  LABIALIS   (HERPES  SIMPLEX). 

This  consists  of  a  vesicular  eruption  upon  the  lip,  tongue,  mouth, 
cheeks,  or  alte  of  the  nose.  The  vesicles  are  filled  with  a  clear  fluid 
which  soon  discharges.  An  excoriation  is  left  often  covered  by  a 
light  crust,  which  is  never  followed  by  a  scar.  The  condition  may 
cause  little  pain  or  considerable  burning  and  itching.  It  may  accom- 
pany colds,  fevers,  exposure  to  heat,  draughts,  and  gastric  disorders. 
It  follows  either  a  direct  irritation  of  the  nerves,  as  after  the  use  of 
rubber  dam  or  other  dental  operations  in  susceptible  persons,  or  may 
be  of  reflex  origin;  in  either  case  localized  jjeripherul  neuritis  being 
the  initial  lesion.^     There  is  some  reasou  to  believe  that  infection 

'  Miller,  Dental  CoHinos,  1891.  -  Ibid. 

'  Hyde  and  Montgomery,  Diseases  of  the  Skin. 


LEUKOPLAKIA  BUCCALIS  695 

plays  a  part  in  its  production.  As  a  preventive  it  is  well  to  lubricate 
the  lips  with  glycerin  and  rose  water  or  with  cold  cream  when  much 
stretching  or  other  irritation  is  necessary. 


HERPES  ZOSTER. 

This  is  a  probably  infectious  disease,  almost  invariably  mono- 
lateral,  associated  with  a  neuritis  usually  of  a  spinal  ganglion  or  with 
a  peripheral  neuritis,  which  produces,  first,  a  hyperesthesia  of  the  in- 
tegument, macules,  and  later  vesicular  eruptions  not  usually  begin- 
ning on  a  mucous  surface.  They  appear  in  groups  and  may  coalesce, 
forming  patches.     Desiccation  forms  a  crust;  pus  may  form. 

The  interest  to  dentists  lies  in  the  fact  that  m  zoster  of  the  head 
exfoliation  of  the  teeth  is  said  to  be  associated  in  rare  cases.* 


LEUKOPLAKIA  BUCCALIS. 

Upon  the  inner  surface  of  the  cheeks  or  lips,  and  upon  portions  of 
the  gum  and  the  dorsum  and  edges  of  the  tongue,  may  appear  sharply* 
outlined,  dull,  whitish,  slate-colored  or  silver-whitish  points,  disks, 
streaks,  bands,  ribbons,  or  patches  of  irregular  shape,  either  flattened 
or  slightly  elevated,  above  the  general  level  of  the  mucous  surface. 
They  may  crack  or  fissure,  and  inflammation  of  the  derma  and  pain 
result.  Ordinarily  they  are  simply  rough  and  without  much  dis- 
comfort. It  occurs  almost  exclusively  in  males.  They  differ  from 
the  mucous  patches  of  syphilis  in  that  the  latter  are  soft  and  tend  to 
ulcerate,  and,  while  they  may  accompany  syphilis,  may  occur  in  its 
absence  or  of  any  history  of  it. 

They  simulate  the  keratosis  of  lichen  planus,  which  should  also 
appear  as  papules  upon  other  parts  of  the  body. 

Apart  from  syphilis,  it  is  due  to  irritation  such  as  that  from  tol)acco 
or  rough  teeth,  and  with  syphilis,  tobacco  and  rough  teeth  may  be 
additional  excitants. 

The  use  of  alcohol  and  spices  are  also  a  cause. 

The  ])elli('le  is  closely  adherent,  and  consists  of  an  hyjMM-tropliIed 
and  hyperkeratinized  epithelium,  with  more  or  less  intiainnuitory 
infiltration  of  the  derma  and  with  partial  obliteration  of  tlie  papilhr. 

'  Hyde  and  AFoiitgomery,  Diseases  of  tlie  Skin. 


696  INFECTIONS  OF  AND  FROM  THE  MOUTH 

The  chief  danger  m  the  disease  is  the  tendency  to  epithehoma, 
especially  in  the  cases  m  which  exfoliation  and  ulceration  occur. 

The  removal  of  the  pellicles  by  suitable  caustics,  galvanocautery,  or 
bur,  and  the  avoidance  of  all  irritants,  especially  tobacco  and  alcohol, 
and  the  use  of  soothing  mouth  washes,  together  with  a  hygienic  regi- 
men, is  the  usual  treatment  to  avoid  epithelioma.  The  diagnosis  lies 
clearly  within  the  province  of  the  dentist  who  may  note  it  before  the 
patient.     The  treatment  is  usually  conducted  by  the  physician. 

Syphilic  cases,  of  course,  require  antisyphilitic  treatment,  especially 
with  mercury. 

Leukoplakia  has  been  also  called  buccal  psoriasis,  but  psoriasis  does 
not  affect  mucous  surfaces,  hence  it  is  a  misnomer. 


LICHEN  PLANUS. 

This  condition,  which  may  simulate  leukoplakia,^  is  characterized 
by  an  eruption  consisting  of  glistening  flat-topped  polygonal  papules 
with  tendency  to  form  irregularly  arranged  groups.  On  the  mucous 
surface  they  appear  as  whitish  macules,  strife,  or  flat  papules  on  both 
sides  of  the  tongue  at  the  points  in  contact  with  the  molar  teeth. 

They  are  the  result  of  an  arterial  or  venous  hyperemia  of  the 
papillae  of  the  corium,  a  secondary  thickening  of  the  lower  part  of 
the  rete,  and  a  tertiary  flattening  of  the  papule  by  pressure. 

A  proliferation  of  cells  in  the  granular  layer  and  a  deposit  of  kerato- 
hyalin  in  whitish  spots  occurs.  This  causes  a  similarity  to  leukoplakia. 
It  usually  occurs  in  the  nervously  exhausted,  though  many  patients 
may  have  a  fair  degree  of  body  nutrition  while  yet  nervously  ex- 
hausted. 

PHOSPHOR  NECROSIS. 

This  disease  is  a  more  or  less  extensive  necrosis  of  tlie  maxillse  due 
to  the  entrance  of  phosphorus  or  its  fumes  into  contact  with  the 
periosteum  or  pericementum  of  a  tooth. 

It  was  formerly  frequent  in  match  factories,  but  has  occurred 
through  the  chewing  of  match  heads. 

As  it  does  not  ordinarily  occur  in  the  mouths  of  those  having  sound 
teeth,  it  is  generally  regarded  as  of  local  origin,  the  phosphorus  gaining 

'  Ilyde  and  Montgomery,  Diseases  of  the  Skin. 


ANGINA  697 

entrance  either  through  the  pulp  canal  of  a  tooth,  or,  possibly,  through 
some  point  of  injury  external  to  the  tooth. 

Abscesses  containing  offensive  pus  cause  great  swelling  and  exces- 
sive salivation,  and  may  cause  several  fistulas,  while  the  swallowing 
of  the  discharge  causes  general  toxic  disturbance,  and  infection  such 
as  pneumonia  or  cerebrospinal  meningitis  may  have  rapid  effect. 

The  periosteum  remauis  unaffected  as  to  its  vitality,  while  the  bone 
proper  undergoes  osteoporous  necrosis,  becoming  like  rotten  sponge. 
As  the  sequestrum  is  separated,  there  is  a  tendency  to  formation 
of  new  bone  by  the  periosteum.  The  necrosis  of  bone  may  be  very 
extensive,  involving  in  the  lower  jaw  the  entire  horizontal  portion, 
while  the  ramus  may  remain  unaffected.  In  the  lower  jaw,  after 
exfoliation,  the  bone  may  be  almost  entirely  restored  to  an  amount 
nearing  fair  comparison  with  the  ordinary  edentulous  mouth,  while 
in  the  upper  jaw  no  repair  occurs.  This  new  bone  may  undergo 
atrophy  if  not  put  to  work  by  artificial  teeth. ^ 


ANGINA. 

Angina  is  usually  defined  as  a  sense  of  choking  or  suffocation, 
a  symptom  which  accompanies  inflammatory  affections  of  the  pharynx 
as  well  as  the  paroxysmal  neuralgic  affection  of  the  heart  known  as 
angina  pectoris. 

Angina  Simplex.^ — This  is  inflammation  of  the  pharynx,  with,  of 
course,  more  or  less  swelling  and  infiltration  of  exudate.  Swallowing 
may  be  diflScult.  Local  depletion  and  sedation  washes,  with  general 
derivation,  are  indicated.  If  chronic,  stimulant  washes  are  useful 
combined  with  general  tonic  treatment. 

Ludwig's  Angina. — In  1836  Ludwig  described  a  disease  which 
is  considered  to  be  an  infectious  cellulitis  in  the  submaxillary  region. 
The  infection  thought  to  be  due  to  the  Streptococcus  pyogenes  or 
bacillus  of  malignant  edema  probably  enters  the  cellular  tissue  of  the 
submaxillary  region  and  neck  through  the  oral  or  pharyngeal  mucous 
membrane  or  a  wound.  The  patient  has  lassitude,  chilliness,  and 
fever. 

A  hard  swelling  appears  beneath  the  mandible  after  several  days, 
and  extends  toward  the  neck  and  under  the  tongue.  The  skin  is  not 
much  reddened. 

'  For  consideration  of  treatment  the  reader  is  referred  to  Garretson'a  System  of  Oral 
Surgery,  sixth  edition,  and  other  writings  upon  the  subject. 


698  INFECTIONS  OF  AND  FROM  THE  MOUTH 

Breathing  and  swallowing  are  rendered  difficult.  Upon  incision 
the  connective  tissues  are  found  to  be  sloughmg,  grayish  black  in  color, 
and  may  ooze  pus. 

The  spread  of  the  infection  being  by  continuity  of  cellular  spaces, 
the  glands  are  not  much  enlarged. 

A  large  abscess  may  form  and  discharge.  Pneumonia,  septicemia, 
and  pyemia  are  complications  to  be  feared.  Incisions  for  drainage 
and  antisepsis  are  usually  conjoined  with  systemic  treatment. 


DENTAL  STERILIZATION. 

It  must  ever  be  borne  in  mind  that  the  dental  operator  constantly 
works  in  a  field  of  infection,  and  unless  extraordinary  precautions  be 
taken  every  instrument  which  touches  this  field — the  fingers  of  the 
operator,  his  mirrors,  glasses,  napkins,  rubber  dam,  rubber  dam 
clamps — ^becomes  immediately  infected  as  soon  as  it  is  brought  in 
contact  with  the  mouth  of  the  patient.  The  likelihood  of  infection 
varies  with  the  patient  and  the  particular  instruments;  mouth  mirrors, 
rubber  dam  clamps,  scalers,  and  all  instruments  used  in  the  treatment 
of  pulp  canals  are  likely  to  become  more  promptly  and  extensively 
infected  than  other  instruments.  Again,  the  forms  of  the  instruments 
determine  whether  or  not  increased  opportunity  is  given  for  the  reten- 
tion of  infective  material.  The  fingers  of  the  operator  may  be  the 
medium  through  which  infective  material  is  transferred  from  one 
patient  to  another.  Infection  may  be  carried  from  superficial  areas 
of  the  mucous  membrane  of  the  mouth,  from  the  enamel  and  the 
saliva,  into  deeper  structures,  where  conditions  are  favorable  for  the 
development  of  sepsis. 

The  scheme  for  dental  sterilization,  therefore,  includes  the  steriliza- 
tion of  the  operator,  instruments,  apparatus,  appliances,  etc.,  used  in 
ojK'rations,  and  the  sterilization  of  the  field  of  operation  prior  to 
operating. 

The  Operator. — Extreme  personal  cleanliness  upon  the  part  of  an 
operator  is  cleai'ly  the  first  step  in  asepsis.  The  best  class  of  dentists 
are  exceedingly  neat  as  regards  personal  habits:  daily  bathing,  care  of 
the  nails  and  of  the  skin,  and  immaculate  linen  form  as  much  a  part 
of  the  day's  labor  as  dental  operations  per  se.  The  virtues  of  soap 
and  water,  wherever  they  may  be  apj)lied,  are  regarded  as  a  vei'y 
important  item  in  preventing  infection. 


DENTAL  STERILIZATION  699 

Linen  which  has  been  boiled  prior  to  wearing  may  be  regarded  as 
safely  sterile;  so  that  the  matter  of  personal  sterilization  relates  to  the 
hands,  particularly  to  the  finger-nails.  The  space  under  the  nails  is 
a  favorable  habitat  for  many  organisms,  notably  the  pyogenic  cocci, 
the  Staphyloccus  pyogenes  aureus  being  commonly  present  in  this 
situation. 

It  has  always  been  advised  that  the  finger-nails  be  trimmed  short, 
and  be  made  smooth  to  avoid  mechanical  injury  to  the  soft  tissues  of 
the  patient.  Since  the  advent  of  aseptic  and  antiseptic  surgery  these 
precautions  have  an  additional  significance;  nails  kept  short  and 
smooth  may  be  more  readily  cleansed  than  if  long  and  ill-kept.  The 
nails  should  be  cut  so  that  they  nowhere  project  beyond  the  tips  of 
the  fingers.  Their  mechanical  cleansing  should  be  done  with  smooth 
instruments,  not  sharp  knife  blades;  the  latter  produce  rough  surfaces, 
which  furnish  spaces  for  lodgement  of  bacteria.  There  is  ])ut  one 
effective  method  of  washing  beneath  the  nails;  it  is  that  followed  by 
the  general  surgeon :  after  dipping  the  soap  in  water  as  hot  as  can  be 
borne  by  the  hands,  all  of  the  finger-nails  should  be  made  to  scrape  the 
soap  until  the  spaces  under  the  nails  are  filled  with  soap.  After  this 
coarse  hand-brushes  are  used  to  scour  every  part  of  the  hands  with 
soap  and  water  as  hot  as  can  be  borne.  Special  nail-brushes  are  next 
used  to  scrub  beneath  the  nails,  driving  out  piecemeal  the  soap  masses 
there.  The  general  surgeon  continues  the  scrubbing  until  the  nails 
are  scrupulously  clean.  The  soap  usually  used  is  Castile,  or  soap 
made  from  palm  oil,  etc.,  but  antiseptic  soaps,  such  as  ethereal  soaps, 
may  be  substituted  with  advantage. 

Sterilization  of  the  cleansed  hands  is  insured  by  immersing  them 
for  five  minutes  in  antiseptic  solutions,  such  as  a  1  to  2000  solution  of 
mercuric  chloride.  The  hands  should  be  sterilized  after  treating  each 
patient;  rubbing  the  hanils  with  a  paste  of  flour,  mustard,  and  water 
for  three  minutes  and  washing  oft'  with  sterilized  water  is  eft'ective 
(Nancrede).  If  the  patient  dismissed  has  possessed  an  unusually 
septic  mouth,  or  has  been  a  syphilitic,  for  example,  the  time  I'oi- 
hand  cleansing  and  sterilization  is  to  be  prolonged;  if  syphilitic, 
every  instrument  used  is  transferred  to  separate  vessels  containing 
antiseptic  solutions  or  boiled,  and  the  hands  are  viewed  as  highly 
infected;  they  are  scrubbed  with  mercuric  chloride  solutions  to 
prevent  personal  infection  or  the  carriage  of  infection.  Chancres 
have  from  time  to  time  appeared  upon  the  fingers  of  tlentists  as 
well  as  physicians. 


700  INFECTIONS  OF  AND  FROM   THE  MOUTH 

Sterilization  of  Apparatus. — The  scrupulous  cleanliness  of  the 
operating  chair,  whose  head-rest  should  receive  frequent  changes  of 
boiled  linen  coverings,  metallic  parts  rubbed,  and  general  covering 
cleansed;  the  cleansmg,  polishing,  and  sterilizmg  of  cuspidores;  the 
changing  of  paper  covermgs  upon  instrument  tables,  etc.,  are  part  of 
the  general  scheme  of  sterilization.  The  floor  of  the  operating  room 
also  requires  attention;  instead  of  being  covered  with  carpet,  it  is 
preferable  to  have  it  made  of  parquetry  material  or  cement,  over 
which  rugs  are  laid,  which  may  be  removed  from  the  room  for  cleans- 
ing, the  floor  proper  being  scrubbed. 

Napkms  used  about  the  mouth  are  certam  to  become  infected,  so 
that  their  boiling  should  be  prolonged  at  least  fifteen  minutes.  For 
many  operations  it  is  preferable  to  substitute  strips  of  muslin  for  linen 
napkins,  which  after  being  used  may  be  thrown  away. 

If  a  hydraulic  saliva  ejector  be  used,  the  glass  mouth  tubes  should 
be  changed  for  each  person,  a  sterilized  tube  being  substituted  directly 
before  its  use  is  required.  A  number  of  these  tubes  should  be  in  use, 
and  may  be  sterilized  after  washing  by  placing  them  in  a  50  per  cent, 
solution  of  listerme  or  a  formaldehyde  solution  for  a  few  hours. 
Tumblers  and  mouth  mirrors  may  be  sterilized  in  like  manner.  The 
cloudiness  of  saliva  tubes  is  produced  by  the  formation  of  salivary 
calculus,  and  may  be  removed  by  the  use  of  acidulated  water.^ 

At  the  close  of  each  day  a  large  cup  should  be  filled  with  an  anti- 
septic solution,  which  is  to  be  drawn  through  the  tubing  of  the  ejector 
to  keep  it  in  a  reasonably  aseptic  condition. 

Rubber  dam  may  be  sterilized  by  boiling  water,  but  it  is  more  safe 
and  cleanly  to  use  a  new  piece  for  each  patient.  It  should  be  washed 
and  then  dusted  with  borated  talcum  powder.  The  possibilities  of 
infection  through  this  medium  are  great,  particularly  in  syphilitic 
cases. 

The  water  used  for  douching  cavities  should  be  boiled  previous  to 
placing  in  the  warmer,  and  should  have  a  little  pleasant  antiseptic 
added  to  it. 

Nancrede^  states  that  all  pyogenic  cocci,  and  even  anthrax  spores, 
are  killed  by  boiling  instruments  for  two  minutes  in  a  1  per  cent, 
solution  of  sodium  carbonate,  which  also  prevents  rusting. 

Mouth  mirrors  and  other  instruments  which  can  be  wet  may  be 
placed  for  one-half  hour  or  longer  in  a  covered  jar  containing  20  per 

'  Thornton,  Dental  Review,  1903. 

2  Park's  Surgery  by  American  Authors. 


DENTAL  STEETLIZATION  701 

cent,  formaldehyde,  to  which  borax  has  been  added  to  saturation. 
Rusting  is  prevented  by  borax  (WiUiams). 

Broaches,  trephines,  and  other  small  points  requiring  to  be  kept 
sterile  may  be  placed  in  a  bottle  such  as  are  sold  containing  gold 
cylinders,  and  kept  wet  with  any  essential  oil  or  carbolic  acid. 

G.  Zederbaum^  suggests  sticking  the  shanks  in  the  cork;  when  to  be 
used  the  cork  is  to  be  transferred  to  another  bottle  of  like  size  contain- 
ing alcohol  and  shaken  to  remove  the  antiseptic. 

Extracting  forceps  require  careful  mechanical  cleansing  and  jiro- 
longed  boiling  after  each  use,  for  perhaps  more  cases  of  infection, 
and  of  many  kinds,  have  resulted  from  unclean  forceps  than  from 
all  other  causes  combined. 

Instruments,  such  as  hand-pieces,  which  cannot  be  conveniently 
wet  may  be  subjected  for  ten  minutes  to  formaldehyde  gas,  de- 
veloped in  a  Low  or  Schering  apparatus.^  If  desired,  all  the  instru- 
ments may  be  so  sterilized.  The  entire  instrument  case  may  be 
disinfected  by  burning  a  Low  lamp  in  one  drawer  of  the  dental  cabinet 
for  one-half  hour  at  night.  The  drawers  should  be  made  communi- 
cating by  small  perforations  at  one  or  more  points.  iNIiller  found 
that  placing  a  formalin  tablet  in  each  drawer  sufficed  to  sterilize  its 
contents. 

Sterilizing  the  Field  of  Operation. — To  insure  sterilization  of  the 
field  of  operation  antiseptics  should  be  used  freely  about  the  mouth 
prior  to  operating.  The  thoroughness  of  the  sterilization  will  depend 
in  great  degree  upon  the  personal  habits  of  the  patient.  If  by  the 
systematic  use  of  the  agents  and  measures  described  under  the  prophy- 
laxis of  caries  the  patient's  mouth  be  kept  in  a  reasonably  aseptic 
condition,  sterilization  of  the  oral  cavity  can  be  accomplished  with 
sufficient  readiness.  The  choice  of  antiseptic  will  depend  in  great 
degree  upon  the  state  of  oral  hygiene;  in  ill-kept  mouths,  with  deposits 
of  foreign  materials  about  and  between  the  teeth,  on  the  gums  and 
tongue,  much  more  active  and  penetrating  germicides  will  be  required 
than  if  the  parts  are  clean.  The  presence  of  putrefactive  decom- 
position in  the  mouth,  made  evident  by  ill  odors,  amid  which  that  of 
hydrogen  sulphide  may  be  detected,  needs  for  its  treatment  the 
immediate  and  free  use  of  preparations  from  which  nascent  oxygen 
may  be  disengaged.  A  good  method  is  to  forcibly  spray  the  mouth 
with  a  1  to  3  per  cent,  solution  of  hydrogen  dioxide,  in  order  to  force 
infective  material  from  about  the  teeth.     The  otlier  solutions,  as  a 

^     1  Dental  Cosmos,  1907.  ^  See  .\inerican  Text-book  of  Operative  Dentistry. 


702 


INFECTIONS  OF  AND  FROM   THE  MOUTH 


solution  of  potassium  permanganate  or  mercuric  chloride  (see  p, 
397),  may  then  be  used.  This  spraying  should  be  somewhat  pro- 
longed when  the  mucous  membrane  is  likely  to  be  injured.  Many 
operators  keep  a  stock  of  inexpensive  tooth-brushes  for  such  cases, 
which  are  thrown  away  after  the  patient  has  used  them,  who  is  directed 
to  scrub  the  teeth  well  with  the  brush  and  the  antiseptic  solution. 


Fig.  567 


Low  sterilizer:  A,  sterilizing  chamber;  £,  perforated  tray  on  which  instruments  to  be 
sterilized  are  placed;  C,  glass  dome  and  cast  aluminum  support;  O,  condensing  chamber 
for  removing  all  moisture  from  gas;  D,  formaldehyde  burner;  E,  platinum  cone,  which 
generates  the  gas  from  Columbian  spirit;  F,  lamp  body.  The  course  of  the  gas  through 
the  apparatus  is  indicated  by  the  arrows. 


For  very  thorough  disinfection  thoroughly  cleanse  the  teeth  and 
use  the  antiseptic  between  them  upon  floss  silk.  For  surgical  work 
or  etherization  very  active  work  should  be  done.  Wadsworth,*  in 
an  investigation  of  mouth  washes  and  their  action  on  pneumococci, 
found  but  little  value  in  the  ordinary  wash  or  even  solutions  of 
formalin,  lysol,  or  HgOg.     He  fomid  that 


I^. — Alcohol 

Water 

Glycerin  and  salt,  a  small  quantity  added. 


30  parts 
70  parts 


was  very  effective  in  destroying  the  bacteria. 

The  routine  practice  of  scaling  and  polishing  the  teeth  and  pre- 
scribing an  antiseptic  mouth  wash  prior  to  the  commencement  of  a 
series  of  sittings  is  to  be  highly  commended. 

Before  scaling  absolute  disinfection  is  impossible.  The  writer 
uses  the  antiseptic  freely  during  the  entire  operation. 

'  Dental  Cosmos,  1907. 


DENTAL  STERILIZATION  703 

If  ulcerations  or  inflammatory  conditions  exist,  tlie  sterilization  is 
to  be  prolonged.  If  a  suspicion  of  syphilis  exist,  not  only  should  the 
mouth  be  freely  washed  with  strong  antiseptics,  but  special  instru- 
ments should  be  used,  preferably  an  old  set,  kept  sterilized  and  used 
only  in  special  cases.  If  the  hands  of  the  operator  have  abrasions 
or  irritated  spots,  these  should  be  covered  with  collodion,  and  after 
the  operation  should  be  carefully  sterilized  to  prevent  personal  infec- 
tion, of  which  a  number  of  cases  have  been  recorded.    (Sec  p.  689.) 

A  deep  infection  may  usually  be  prevented  during  the  treatment 
of  pyorrhea  alveolaris  and  pulp  gangrene  by  attention  to  the  steril- 
ization of  the  infected  tract  before  beginning  work  upon  the  parts 
or  during  its  progress.  These  methods  have  been  indicated  in  the 
discussion  of  these  subjects. 


IxXDEX. 


Abrasion  in  animals,  278 

of  calculus,  271 

degrees  of,  271 

effects  of,  277 

from  clasp,  276 

gritty  powders  as  cause  of,  272 

labial  and  approximal,  272,  276 

lingual,  273 

occlusal,  270 

relation  to  caries,  277 

tooth-brush  in,  272,  275 

treatment  of,  279 
Abscess,  apical,  acute,  516.     See  Peri- 
cementitis, 
chronic,    535      See    Perice- 
mentitis, 
scar  from,  552 

extraction  in  second  stage  of,  532 

fistula  in,  125 

pericemental,  657 
diagnosis  of,  664 
morbid  anatomy  of,  662 
symptoms  of,  662 
treatment  of,  665 

pointing  in,  125,  127 

of  pulp,  448 

pus  in,  126 
AcetaniUde,  use  of,  362,  443,  529,  671 
Acidosis,  acids  in,  86,  94,  95 
Aconite,  dental   tincture  of,  116,   210, 

429,  527,  567 
Actinomycosis  of  mouth,  692 
Aerogenic  bacteria,  42,  43 
Adrenalin,  use  of,  364,  367 
Agenesia  of  enamel,  230 
Agglutination,  57 
Albumin,  fermentation  of,  44 
Albuminuria,  104 
Alcohol,  injection  of,  678 

use  of,  361,  381,  595,  596,  685 
Alexins,  50 

Aloin  compound,  use  of,  603 
Alopecia,  from  dental  disease,  677 
Alum,  use  of,  442,  459,  488,  492,  495,  646 
Alveolar  process,  fracture  of,  589 
Alveolitis,  postextraction,  573,  589 
Amalgam,  copper,  use  of,  382,  503 

facing,  476 
Amboceptors,  56 
Ameba,  properties  of,  18 
Ameloblasts,  152 

45 


Ammonium  carbonate,  use  of,  370 
Ammonol,  use  of,  362 
Amputation  of  roots,  389 

of  root  end,  530 
Anemia,  105,  106,  107,  108 
Anaesthesia,  general,  use  of,  361,  442, 
466 
by  pressure,  442, 447,  452 

of  the  pulp,  467 
Angina,  Ludwig's,  697 

simplex,  697 
Ankylosis,  dental,  573 
Antikamnia,  use  of,  362 
Antipyrin,  use  of,  678 
Antiseptic  powders,  use  of,  129 
Antiseptics,  mouth,  396 
Antitoxin,  formation  of,  56 

streptococcus,  use  of,  142 
Antrum,  empyema  of,  550,  551 
Aphtha,  685' 
Aqua  regia,  use  of,  483 
Argyrol,  use  of,  647 
Aristol,  use  of,  129,  381,  485 
Arsenic,  accidents  with,  479 

coverings  for,   476 

iodide  of,  use  of,  439 

pocket  for,  477 

second  application  of,  476 

use  of,  418,  443,  447,  452,  471 
danger  of,  372,  465,  479 
Arsenical  fiber,  474 
Arterial  hyperemia,  114 
Arteriosclerosis  of  pulp,  453 
Asbestos,  use  of,  381,  391,  497 
Ascher's  enamel,  use  of,  382 
Atrophy,  72 

general,  72,  90 

local,  72 

marginal,  of  gum,  603 

Harlan's  method  in,  604 
Atropine,  use  of,  361,  569,  684 
Attachment  of  teeth,  589 
Auto-intoxication,  causes  of,  85 

general    malnutrition   as 
causes  of,  90 

oral  effects  of,  568 


B 


Bacteria,  action  of  gastric  juice  upon, 
48,50 
aerogenic,  42,  43 


706 


INDEX 


Bacteria,  in  blood,  46 

as  cause  of  disease,  35 

of     inflammation,     123,     125, 
126,  127 

chemical  composition  of,  38 

chromogenic,  42 

destruction  of,  by  tissue,  50 

division  in  blood,  41 

effect  of  blood  reaction  upon,  57 

external  antagonistic  agencies,  58 

facultative,  42 

fermenting  action  of,  42 

ferments  of,  43 

forms  of,  39 

immunity  to,  52,  56 

intoxication  by,  92 

life  conditions  of,  39 

localization  of,  49 

media  of,  39 

motility  of,  38 

of  mouth,  47,  49  _ 

general  infection,  by,  49 

obligate,  42 

parasitic,  41 

pathogenic,  41,  45,  47 

penetration  of  root  tubules  by,  559 

position  in  vegetable  kingdom,  35 

predisposition  to,  action  of,  29,  48 

P3'ogenic,  46 

saprophytic  41,  44 

specific,  45 

spore  formation  of,  40 

spreading  of,  in  tissue,  46 

toxic  effects  of,  41 

universality  of,  45 

zooglea  of,  40 
Bacterial  plaques  in  dental  caries,  312, 

313 
Band,  dental,  151 
Benzoic  acid,  use  of,  595 
Bilein,  use  of,  603 
Bismuth,  subnitrate,  use  of,  195 
Black,  glands  of,  178 
Black's  1-2-3  mixture,  use  of,  647 

operation  for  scar,  552 
Blastomycetes,  36 

in  stomach,  49 
Bleaching  agents,  use  of,  510 
Blindness,  dental,  cause  of,  572 
Blood,  bacteria  in,  46 

coagulation  of,  108 

extravasation  of.  111 

pressure  of,  182 

reaction  of,  as  immunizing  factor, 
57 

supply  to  teeth  and  jaws,  177 
Blooflletting  in  inflammation,  etc.,  118, 

130,  129 
Blue  light,  use  of,  362,  561,  678 
Bone,  caries  of,  82,  135 

of  face,  embryology  of,  145 

infection   of,  from    dental  lesions, 
553 

inflammation  of,  134,  553 

of  jaw,  development  of,  156 

necrosis  of,  136 


Bone,  necrosis  of,  from   alveole   dental 
abscess,  555 
from  syphilis,  556 
regeneration  of,  137 
resorption  of,  135,  136 
in  gingivitis,  601 
Boric  acid,  use  of,  596,  678 
Boroglycerin,  use  of,  595 
Brandy,  use  of,  194 
Brewers'  yeast,  use  of,  129 
Broaches,  Downie,  use  of,  560 

varieties  of,  uses  of,  482,  488 
Brush,  use  of,  646 
Bruxomania,  271 


Caffeine,  use  of,  529,  678 
Calcareous  infiltration,  79 
Calcific  degeneration  of  pulp,  419 
Calcium  chloride,  use  of,  113 
phosphate,  use  of,  557 
salts  in  blood,  609 
origin  of,  609 
in  pus,  623 
Calcoglobulin,  80,  155 
formation  of,  85 
Calcospherites,     chemical    composition 
of,  155 
■    function  of,  154,  155 
in  pericementum,  180 
Calculi,  basis  of,  80 
Calculus,  analyses  of,  60S 
hematogenic,  623 
origin  of,  607 
pyogenic,  623,  658 
salivary,  606 

foreign  bodies  in,  610 

hardening  of,  613 

mode  of  deposit,  612,  614 

of  formation,  611 
occurrence  of,  607 
origin  of,  607 

pathological  effects  of,  614 
prognosis  of,  615 
recurrence  of,  620 
removal  of,  615 
scalers  for,  616,  622 
structure  of,  610 
treatment  of,  615 
varieties  of,  607 
sanguinary,  623 
stroma  of,  608 
subgingival,  620 
causes  of,  620 
effects  of,  621 
removal  of,  623 
scalers  for,  622 
symptoms  of,  621 
treatment  of,  623 
varieties  of,  606 
Calendula,  use  of,  595 
Calisaya,  use  of,  569 
Calomel,  use  of,  602 
Campho-phenique,  use  of,  647 
Canada  balsam,  use  of,  381 


INDEX 


r07 


Canals,  imperfcctl}-  filled,  results  of,  558 

Cancrum  oris,  686 

Cantharides,  use  of,  470 

Capping,  for  pulp,  385 

Capsicum  plaster,  use  of,  529 

Carbolic  acid,  use  of,  194,  368,  370,  371, 

376,  442,  470,  567,  647 
Carbon   dioxide,    defective  elimination 
of,  88 
paper,  use  of,  583 
Carcmoma,  70 
Caries  of  bone,  82,  135,  543 
dental,  304 

acids  in,  lactic,  338 

neutralization  of,  336 

age  in, 320,  352 

alkalies  in,  312 

bacterial  plaque  in,  312,  313 

bodily  condition  in,  321 

causes  of,  bacterial,  307,  310, 
339 
exciting,  304,  307 
predisposing,  local,  314 
systemic,  318 

in  cementum,  345,  352 

chemical  reactions  in,  310 

deep  seated,  370 

dentine  in,  332 

secondary,  352 

diagnosis  of,  354 

eburnation  in,  343 

effect  of  malnutrition  upon,  88 

in  enamel,  324 

experiments  in,  307 

filth  as  a  protection  from,  322 

foodstuffs,  in,  310 

heredity  in,  319 

history  of,  304 
clinical,  345 

inception  of,  323,  345 
locations  of,  323 

lactates  formed  in,  337 

liquefaction  foci  in,  338 

loss  of  crown  by,  388 

morbid  anatomy  of,  323 

mucin  in,  316 

of  Nasmyth's  membrane,  332 

pathology  of,  323 

perforation  by,  386 

pigmentation  in,  343 

prognosis  of,  355 

prophylaxis  of,  394 

pulp  in,  almost  exposed,  379 
exposed,  383 

recurrence  of,  393 

self-healed,  351 

simple,  375 

stages  of,  374 

structure  of  teeth  in,  317 

superficial,  374 

symptoms  of,  354 

of  temporary  teeth,  390 

terminations  of,  353 

therapeutics  of,  374 

transparent  zone  in,  341 

tube  casts  in,  340 


Caries,  dental,  under  fillings,  340 

Caseation,  75 

Cassia,  oil  of,  use  of,  596,  605 

Castor  oil,  use  of,  195,  678 

Catabolism,  23 

Cataphoresis  as  test,  365,  496,  547 

in  hypersensitive  dentine,  365 
Cataplasma  kaolini,  use  of,  220,  530 
Cautery,  electric,  use  of,  373 
Cells,  chemical  changes  in,  23,  24 

composition  of,  17 

giant,  60 

hypertrophy  of,  60 

life  conditions  of,  24 

movements  of,  19 

nucleus  of,  18 

properties  of,  19 
phagocytic,  19 

receptors  of,  23,  54 

reproduction  of,  19 

stimulation  of,  effects  of,  59 

stimuli  of,  20 
Celulitis,  submaxillary,  697 
Cement,  development  of,  153 

substance,  interprismatic,  155 

oxychloride  of  zinc.     See  Zinc. 

oxphosphate  of  copper.  See  Copper. 

oxysulphate  of  zinc.     See  Zinc. 

silicate,  use  of,  383 

zinc  phosphate.     See  Zinc. 
Cementum  in  dental  caries,  345,  352 

formation  of,  157,  158 

histology  of,  170 

malformations  of  microscopic.  231 

relation  of,  to  enamel,  164,  170 
Chalk  mixture,  use  of,  195 
Chemotaxis,  51 
Chloral,  use  of,  362 

hydrate,  use  of,  441 
Chlorine,  use  of,  302,  510,  511 

nascent,  use  of,  506 
Chloroform,  use  of,  201,  219,  367,  442, 

447,  488,  567 
Chloropercha,  use  of,  381,  487 
Chlorophyll,  chemical  action  of,  37 
Chlorosis,  105,  107,  114 
Chorea  from  dentition,  217,  672 
Chromic  acid,  use  of,  371 
Chromogenic  bacteria,  42 
Cinchona,  use  of,  64() 
Cinnamon,  oil  of,  use  of,  195,  646,  647 
Circulation,  disturbances  of,  105 

local,  113 
Cleft  palate,  embryology  of,  148 
Clot,  absorption  of,  133 

septic,  133 
Cloudv  swelling,  75 

Cloves,  oil  of,  use  of,  372,  385,  428,  596 
Coagulation  of  blood,  108 

necrosis,  83 
Coagulants,  use  of,  368 
Cocaine,  use  of,  364,  366,  368,  377,  418, 
441,  447,  466,  467,  469,  493,  530,  567, 
573,  635 
Cold,  use  of,  129,  193 
Collateral  hyperemia,  115 


708 


INDEX 


Colloid  degeneration,  78 
Compensatory  hyperemia,  115 
Complement,  57 
Compress,  use  of,  532,  589 
Concrescence  of  teeth,  241 

diagnosis  of,  218 
Conical  teeth,  234 
Constipation,  dental  pain  from,  677 
Copper  amalgam,  use  of,  382 

ox}-phosphate  of,  use  of,  391,  562 

sulphate,  use  of,  381 
Cotton  root  dressings,  dangers  of,  559 

salicylized,  use  of,  635 

tampons,  danger  of,  553,  554 

use  of,  as  root  fiUing,  488 
Coimterirritants,  use  of,  129,  428 
Counter  pressure  in  opening  tooth,  526 
Crede's  ointment,  use  of,  142 
Creosote,  use  of,  488 
Crowns,  cantilever,  use  of,  388 

removable,  513 
Crypts  of  teeth,  relations  of,  161 
Cusps,  supplemental,  244,  245 
Cysts  associated  with  apical  conditions, 
539 

causes  of,  62 

dental,  561 

dermoid,  62 

teeth  in,  63 

impacted  teeth  as  cause  of,  264 

varieties  of,  61 


Deafness,  dental,  cause  of,  572 
Decalcification  of  teeth,  64,  88 
Degeneration,  73,  79 

calcific,  of  pulp,  419 
cloudy,  of  pulp,  462 
colloid,  78 

of  pulp,  464 
fatty,  of  pulp,  73,  464 
fibroid,  460 

of  pericementum,  586 
hj'aline,  77 

in  mouth,  77 

of  mucous  membrane,  77 
lardaceous,  79 
mucoid,  77 

of  mucous  membrane,  77 
ner\-e-end  of  pulp,  464 
of  pericementum,  579 
Dental  ankylosis,  573 
band,  151 

caries,  304.     See  Caries,  dental, 
follicle,  154 
ridge,  151 
synostosis,  573 
Dentinal  papilla,  151,  153 
Dentine,  bacterial  penetration  of,  443 
in  dental  caries,  332 

secondary,  352 
development  of,  153 
formation  of,  154 
granular  layer  of,  158 


Dentine,  histology  of,  164 
hypersensiti-\aty  of,  355 
causes  of,  357 
diagnosis  of,  361 
pathology  of,  358 
symptoms  of,  359 
treatment  of,  361 
interglobular  spaces  in,  231 
malformations  of,  microscopic,  230 
recalcification  of,  381 
resorption  of,  409,  439,  456 
secondary,  404 

bacterial  penetration  of,  411, 

443 
neuralgia  from,  411 
resistance  to  acid  by,  578 
staining  of,  300,  501 

by  putrefaction,  508 
stains  of,  treatment  of,  301 
tubes  of,  164 

tubular  calcification  of,  403 
Dentition,  cause  of,  181 

constitutional  states  modifying,  202 
normal,  181 
pathological,  186 

as  cause  of  epilepsy,  187 
climate  and  weather  in,  187, 

189 
diet  in,  195, 196 
headache  in,  190 
hemophilia  in,  194 
hemorrhage  after  lancing  in, 

193 
intestinal     complications     in, 
188, 195 
feeding  after,  196 
nervous  disturbances  in,  190, 

201 
paralysis  in,  191 
pulmonary     disturbances     in, 

191 
shock  after  lancing  in,  194 
skin  disorders  in,  191,  194 
strabismus  in,  191 
systemic    conditions   influenc- 
ing, 186,  189 
symptoms  of,  187 
treatment  of,  191  195 
periods  of,  184 
process  of,  183 
second,  203 

disorders  of,  215 
irregularities  of,  208 
necrosis  in,  216 
pathological,  216,  217 
symptoms  of,  185 
Depletion  of  gum,  442 

of  pulp,  344 
Derivation,  use  of,  527,  567 
Dermoid  cysts,  62 

teeth  in,  63 
Diabetes  mellitus,  93,  94 
Diagnosis,  definition  of,  25 

forms  of,  25 
Diathesis,  acquired,  85 
gouty,  95 


INDEX 


709 


Diathesis,  hemorrliagic,  112 

hyperacid,  57,  86 
Dilaceration,  of  teeth,  242 
Disease,  bacterial  causes  of,  35 

basis  of,  21,  24 

causes  of,  27 

clinical  history  of,  25 

existing,  as  a  predisposition,  32 

functional,  25 

predisposition,  to,  29 

previous,  as  a  predisposition,  32 
Discoloration  by  putrefaction  of  pulp, 

508 
Dislocation  of  teeth,  588 
Dobell's  solution,  use  of,  551,  683 
Dover's  powders,  use  of,  527 
Drill,  Beutelrock,  use  of,  500 

Gates-Glidden,  use  of,  560 

spear,  use  of,  526 

use  of,  482 
Drugs,  intoxication  by,  92 
Dry  cups,  use  of,  547 
Dryness,  use  of,  363 
Dwarfism,  of  teeth,  232 


Ear,  disease  of,  from  dental  cause,  672, 

674 
Eburnation  in  dental  caries,  343 
Ecchymosis,  111 

Ehrlich's  theory  of  immunity,  54 
Electricity  as  test,  496 
Electrolysis,  cataphoric,  485,  504 
Emboli,  septic,  110 
Embolism,  110 
Emphvsema  of  cheek  from  air  pressure, 

504" 
Emp3'ema  of  antrum,  551 
Enamel,  agenesia  of,  230 

in  dental  caries,  324 

development  of,  151 

formation  of,  effect  of  exanthemata 
upon,  227 

fracture  of,  291 

histology  of,  164 

tubes,  Caush's,  164,  166 

hypoplasia  of,  228,  234 

lines  of  Schreger  in,  164 

malformation  of,  macroscopic,  226 

I  ::-i  .n  microscopic,  224 

opaque  spots  in,  223 

parts  of,  152 

relation  of,  to  cementum,  164 

resorption  of,  281 

stains  upon,  296 

strife  of,  155,  164 

stripes  of  Retzius  in,  226 
of  Schreger  in,  225 

tubes  of,  164,  166 

unusual  location  of,  244 
Endarteritis  obliterans,  77,  601 
Energy,  nerve,  loss  of,  103 

sources  of,  23,  91 
Ki)ilepsy  from  dental  disease,  672 


Epilepsy,    pathological     dentition      as 

cause  of,  187 
Ergot,  use  of,  113 
Erosion  of  teeth,  282 
acids  in,  283 

extraneous,  287 
causes  of,  282 
diagnosis  of,  290 
effects  of,  288 

malnutrition  upon,  88 
possible    action    of    glvcogen 

in,  76 
systemic  factors  in,  285 
treatment  of,  291 
Eruption  of  teeth,  causes  of,  181 
Escharotics,  effects  of,  565 
Ether,  use  of,  364,  367 
Ethvl  chloride,  use  of,  364, 401,  458,  466, 

528,  530 
Etiolog}^  definition  of,  25,  27 
Eucalyptus,  use  of,  595,  596,  605 
Eugenol,  use  of,  381 
Evans'  root  drier,  use  of,  470 
Exalgin,  use  of,  671 
Exanthemata,  143 

necrosis  caused  by,  144 
Exostosis  of  alveolar  process,  571 
Extravasation  of  blood,  111 
Eye,  disease  of,  from  dental  cause,  672, 
675 


P 


Face,  embryology  of,  145 
Facultative  bacteria,  42 
Fat,  degeneration  of,  73,  79 

infiltration  of,  73 

necrosis  of,  83 
Fermentation,  bacteria  as  causes  of,  38 

definition  of,  42 

of  proteid  matter,  44 
Ferments,  organized,  43 

unorganized,  43 

varieties  of,  43,  44 
Fever,  137 

causes  of,  138 

classes  of,  138 

pathology  of,  138 

prognosis  of,  139 

symptoms  in,  138 

temperature  in,  138 
Fibrin,  formation  of,  108 
Fibrosis  of  pericementum,  580 
Fistulae  in  antrum,  550 

causes  of,  543 

on  face,  threatened,  531 

healing  of,  547 

making  artificial,  528 

packing,  530 

premature  closure  of,  133 
Flagg's  operation  for  scar,  552 
Flexion  of  teeth,  242 
Flora,  normal,  45 
Floss  silk,  use  of,  396,  487 
Follicle,  dental,  154 

waU  of,  153,  158 


710 


INDEX 


Food,  chemical  changes  in,  23 

supply,  abnormal,  27 
Foramen,  open,  treatment  of,  486 
Formo-cresol,  vise  of,  557 
Forma-Percha,  use  of,  488, 497,  506,  538 
Formaldehyde,  action    of,  upon    prod- 
ucts of  putrefaction,  504 
uses  of,  371,  379,  385,  397,  447,  452, 
482,  484,  493,  495,  503,  538,  561, 
596 
Formagen,  use  of,  381,  385,  428,  495 
Fracture  of  alveolar  process,  589 
of  teeth,  291 

repair  of,  294 

reunited,  409 

treatment  of,  294 

Fungi,  as  ferments,  37 

vegetable,  35,  36 

Fusion  of  teeth,  237 


G 


Gallstones,  origin  of,  607 
Gangrene,  82,  83 

circumscribed,  83 
dry,  83 
moist,  83 
of  pulp,  495 
dry,  495 
moist,  498 
partial,  502 
Galvanism,  sterilization  by,  505 
Gastric  juice,  action  of,  on  bacteria,  48, 

50 
Gaultheria,  oil  of,  use  of,  596,  647 
Gelatin,  use  and  danger  of,  113 
Germicides,  action  of,  58 
Giant  cells,  60 
Giantism  of  teeth,  232 
Gingivitis,  591 

antiseptic  washes  in,  595 
astringent  washes  in,  595 
interstitial,  597 
causes  of,  597 
diagnosis  of,  599 
pathology  of,  600 
resorption  of  bone  in,  601 
symptoms  of,  599 
treatment  of,  601 
malnutrition  from,  594 
marginal,  592 
mercurial,  wash  for,  596 
Glands  of  pericementum,  178 
Glycerin,  use  of,  492,  494,  596 
Glycogen,  infiltration  of,  76 
Glycothymolin,  use  of,  596 
Gonorrhea  of  mouth,  693 
Gout,  94,  95 

contrasted  with  rheumatism,  99 
oral  effects  of,  568 
relation  of,  to  teeth,  658 
salts  deposited  in,  80 
Goutiness,  95 

treatment  of,  97 
Granulations  in  regeneration,  130 


Grippe,  dental  pain  from,  677,  678 
Guards  in  pericementitis,  527 
Gum  arable,  use  of,  195 

glycogenic  infiltration  of,  76 
hyperplastic,  458 
laceration  of,  553 
lancing  of,  192,  220 
marginal  atrophy  of,  603 

Harlan's  method  in,  604 
Gutta-percha,   eucalyptol    solution   of, 
use  of,  557 
use  of,  377,  379,  381,  390,  485,  486, 
487,  491,  496,  556 


Halisteresis  ossium,  136 
Hammamelis  distillate,  use  of,  596 
Hands,  sterilization  of,  699 
Harelip,  149,  150 
Headache  in  dentition,  190 

from  pulp  diseases,  671 
Healing  by  second  intention,  130 

under  a  clot,  133 
Heat,  use  of,  129 
Hematogenic  calculus,  623 
Hemoglobin,  derivatives  of,  81 
Hemophilia,  112 

in  dentition,  194 
Hemorrhage,  after  extraction,  589 

local,  treatment  of,  485,  490,  507 

treatment  of,  113 

varieties  of.  111 
Hemorrhagic  diathesis,  112 
Heredity  as  a  predisposition,  32 
Herpes  labialis,  694 

zoster,  695 
Histology,  morbid,  25 
Hoffendahl,  electric  method  of,  505,538 
Hot  water,  use  of,  368 
Hutchinson's  teeth,  235 
Hyaline  degeneration,  77 
in  mouth,  77 

of  mucous  membrane,  77 
Hydrogen  dioxide,  use  of,  129,  194,  302, 

447,  544,  546,  554 
Hydronaphthol,  use  of,  379,  381,  596, 

605 
Hydrastis,  use  of,  113 
Hygiene,  definition  of,  26 
Hyoscyamine,  use  of,  362 
Hyperacidity,  57,  86 
Hyperacidosis,  86,  87 
Hypercementosis,  569 

causes  of,  569 

diagnosis  of,  572 

pathology  of,  570 

reflex  neuroses  from,  572 
pain  from,  672 

situation  of,  570 

symptoms  of,  572 

treatment  of,  573 
Hyperemia,  arterial,  114 

collateral,  115 

compensatory,  115 


INDEX 


711 


Hyperemia,  degrees  of,  115 

as  a  local  predisposition,  115 
pathology  of,  115 
of  pulp,  arterial,  422 

devitalization  in,  430 
from  electric  action,  431 
idiopathic,  430 
thermal  toleration  in,  430 
from  root  resorption,  578 
venous,  432 

devitalization  in,  434 
suffusion  in,  433 
results  of,  115 
symptoms  of,  115 
treatment  of,  116 
venous,  117 

causes  of,  117 
exudate  of,  118 
pathology  of,  117 
treatment  of,  117 
Hypernutrition,  59 

local,  59 
Hyperplasia,  61 

Hypersensitivity  of  dentine,  355 
Hypertropliy,  00 

of  cell,  60 
Hyphomycetes,  36 
Hypnotism,  use  of,  362 
Hypoplasia,  71 

of  enamel,  228,  234 
Hypophosphites,  use  of,  439 


IcHTHYOL,  use  of,  687 
Immunity,  52 
acquired,  52 
and  disease,  29 
Ehrlich's  theory  of,  54 
influences  conferring,  33 
local,  33 
lost,  33 
natural,  52 
Impaction  of  teeth,  256 

as  cause  of  cysts,  264 
death  of  pulp  from,  264 
diagnosis  of,  265 
neuralgia  from,  264 
resorption  of  roots  from,  205 
symptoms  of,  264 
treatment  of,  221,  266 
Inanition,  90 
Indican  as  an  index  of  malnutrition,  88, 

91,  92 
Indol,  91 

Infants,  feeding  of,  196 
Infarction,  111 

of  pulp,  460 
Infection,  classes  of,  46 
of  mouth,  680,  681 
predisposition  to,  29,  30,  33 
resistance  of  tissue  to,  50 
spreading  of,  52 
Infiltration,  calcareous,  79 
dropsical,  78 


Infiltration,  fatty,  73 
glycogenic,  76 
pigmentary,  81 
Inflammation,  bacteria  in,  123,  125,  126, 
127 
bloodletting  in,  81,  129,  130 
of  bone,  134,  553 
causes  of,  1 18 
derivation  in,  116 
exudatesof,  118,  120,  123 
infective,  123 
necrosis  in,  124 
pathology  of,  119,  123 
of  pulp,  435 

chronic,  452 
resolution  in,  121,  123 
simple,  119 
suppurative,  125 
symptoms  of,  122,  127 
general,  123,  127 
treatment  of,  128 
Inoculation  by  bacteria,  45 
Insanity  from  dental  disease,  572,  672, 

676 
Insomnia  from  dental  disease,  677 
Instruments,  sterilization  of,  700 
Intermaxillary  bone,  formation  of,  148 

fracture  of,  150 
Interstitial  gingivitis,  597 
causes  of,  580,  597 
diagnosis  of,  599 
pathology  of,  600 
resorption  of  bone  in,  601 
symptoms  of,  599 
treatment  of,  601 
Intestinal  complications  in  pathological 

dentition,  188,  195 
Intoxication,  intrinsic,  92,  94 

general,  91 
Intubation  of  root,  513 
Iodine,  dental,  tincture  of,  428,  458,  646 

use  of,  371,  507,  527,  619 
Iodoform,  use  of,  129,  485,  489,  512,  547 
lodoformagen,  use  of,  381,  428 
lodoglycerol,  use  of,  602 
Iron,  chloride  of,  tincture  of,  use  of,  529 
Ischemia,  105 


Jaw,  enlargement  of,  cause  of,  161 
Joining  of  teeth,  378 
Jugulation  of  pulp,  433 


Krameria,  use  of,  595 

L 

Laceration  of  soft  tissues  of  mouth, 

589 
Lactic  acid,  use  of,  483,  646 
Lacuna»,  Howship's,  439 
La  grippe  as  cause  of  antral  disease,  551 


712 


INDEX 


Lancing  for  abscess,  529 

gum,  192 
Lardaceons  degeneration,  79 
Laudanum,  use  of,  116,  195 
Lead,  oral  effects  of,  56S 

use  of,  530 

water,  \ise  of,  116 
Leukemia,  105,  107 
Leukocjiiosis,  107,  127 
Leukoplakia  buccalis,  695 
Lichen  planus,  696 
Lime  water,  use  of,  397,  399 
Listerine,  use  of,  195,  596, 686 
Lithemia,  98 

treatment  of,  98 
Liver,  functions  of,  89 

in  general  malnutrition,  89 
Lud-wig's  angina,  697 
Luxation  of  teeth,  588 


M 


Magnesia,  milk  of,  use  of,  372,  397 

sulphate  of,  use  of,  442 
Magnesium  carbonate,  use  of,  646 
Malaria,  dental  pain  from,  666,  677 
Malformations,  macroscopic,  232 

microscopic,  222 

of  roots,  245 

of  teeth,  222 
Malnutrition,  causes  of,  23 

diet  in,  88 

general,  85 

auto-intoxication  in,  90 
cause  of,  86 
diet  in,  88 
liver  in,  89 

from  gingivitis,  594 
Malocclusion  of  teeth,  581 

causes  of,  210 

classification  of,  211 
Malpositions  of  teeth,  254 
Massage  of  abdomen,  use  of,  602 

vibratory,  530 
Maxilla?,  embryology  of,  148 
Maxillary  rampart,  151 
Meckel's  cartilage,  150 
Melancholia  from  dental  disease,  677 
Menthol,  use  of,  363,  367,  371,  441,  447, 

567,  596,  678 
Menthol-phenol,  use  of,  567 
Mercury,  bichloride  of,  use  of,  129,  142, 
396,  485,  492,  529,  546,  549,  554 

as  cause  of  stomatitis,  684 

oral  effects  of,  568 

Talbot's  experiments  on  dogs  with, 
563,  568 
Metabolism,  diseases  of,  85,  90 
Metastasis,  52 

Methyl  chloride,  use  of,  364,  401 
Microorganisms,  as  disease  causes,  35 
Milk,  modified,  196 

Pasteurized,  196 
Morphine,  use  of,  130,  361,  443 
Motor  reflexes  from  dental  disease,  676 


Mouth,  actinomycosis  of,  692 
bacteria  of,  47 

general  infection  by,  49 
pathogenic,  47 
gangrene  of,  686 
gonorrhea  of,  693 
hyaline  degeneration  in,  77  j 
infections  of,  680  ] 

lamp,  electric,  use  of,  496   ' ' 
soft  tissues  of,  laceration  of,  589 
sterilization  of,  701 
syphilis  of,  688,  695,  703 
tuberculosis  of,  692 
washes,  application  of,  596 
Mucin,  characteristics  of,  77 

in  dental  caries,  316 
Mucoid  degeneration,  77 

of  mucous  membrane,  77 
Mucous  membrane,  glycogen  in,  76 
hyaline  degeneration  of,  77 
mucoid  degeneration  of,  77 
overstimulation  of,  effects  of, 
76 
Mummification  of  pulp,  492 
Myrrh,  tincture  of,  use  of,  569,  596 


N 


Nasmyth's  membrane,  156,  164 

in  dental  caries,  332 
Necrobiosis,  81,  82 
Necrosis  of  alveolar  bone,  543 
after  extraction,  533 
of  bone,  136 

from,     alveolodental     abscess, 

555 
from  syphillis,  556 
coagulation,  83 
etiology  of,  82 
of  fat,  83 
liquefaction,  83 
phosphor,  696 
varieties  of,  81 
Neoplasm  of  pulp,  465 
Nerve  energy,  loss  of,  103 
supply,  abnormal,  28 
sensory,  of  face,  668 
trophic  influence  of,  28 
vaso  motor,  114 
Nervocidin,  use  of,  367,  459,  470 
Nervous  disturbances  in  dental  disease, 
666 
in  dentition,  190,  201 
Neuralgia,  dental,  cause  of,  572,  579 
facial,  666,  678 

treatment  of,  078 
from  disease  of  eye,  669 
from  exposed  dentine,  669 
from  impacted  teeth,  264,  673 
from  pulp  disease,  070 
from  secondary  dentine,  411 
in  other  parts  caused   by  dental 
disease,  071,  674 
Neurasthenia,  88,  102,  103 
Neuroses,  reflex,  666 


INDEX 


713 


Neuroses,  reflex,  of  dental  origin,  666 
from  hypercementosis,  572 
of  systemic  origin,  666 
Nitric  acid,  use  of,  371 
Nitrous  oxide  gas,  use  of,  418 
Nodule,  cemental,  232 

in  pulp,  412 
Noma,  686 

Non-conductors,  uses  of,  377,  379 
Nosophen,  use  of,  129 
Nutrition,  basis  of,  22 

deficiency  of,  71 

disturbances  of,  59 

excess  of,  59 


Obligate  bacteria,  42 
Odontoblasts,  153 

atrophy  of,  408,  454 

relation  of,  to  sensrry  nerves,  169 
Odontomata,  246 
Opium,  use  of,  116,  195,  219,  530 
Opsonic  index,  raising  of,  547 
Opsonins,  57 
Organic  matter,  decomposition  of,  37 

fermentation  of,  43,  44 
Organs,  composition  of,  22 
Orthoform,  use  of,  371,  554 
Osteitis,  condensing,  135,  136 

rarefying,  135 
Osteodentine,  410,  439 
Osteomyelitis,  134,  135 
Osteoporosis,  135 
Overfeeding,  91 
Oxaluria,  102 
Oxidation,  deficiency  of,  86 

excessive,  86 
Oxygen,  nascent,  use  of,  506,  510 


Pain,  dental,  from  other  sources  than 
dental,  677 

postextraction,  573 
Palate,  cleft,  cause  of,  148 
Papain,  use  of,  494 
Papoid,  use  of,  129 

Paralysis  from  dental  disease,  572,  672, 
673, 675,  676 

in  dentition,  191 
Parasitic  bacteria,  41 
Paraffin,  use  of,  512 
Paraform,  use  of,  488,  493,  504,  538 
Pathogenic  bacteria,  41,  45,  47 
Pathogenesis,  definition  of,  25 
Pathology,  basis  of,  17,  24,  26 

dental,  definition  of,  17 

general,  definition  of,  17 
Pediluvium,  hot,  use  of,  116 
Peppermint,  use  of,  595,  646 
Perforation  as  cause  of  abscess,  556 

of  root,  491 
Pericemental  abscess,  diagnosis  of,  664 
morbid  anatomy  of,  662 


!  Pericemental  abscess,  symptoms  of,  662 

treatment  of,  665 
Pericementitis,  515        v    ^ 
acute  septic  apical,  516 
causes  of,  517 
clinical  history  of,  522 
diagnosis  of,  524 
pathology  of,  518 
prognosis  of,  525 
SN'mptoms  of,  518 
treatment  of,  525 
complicated,  556 
beginning  at  gum  margin,  591 
chronic,  effects  of,  569 

septic  apical   (non   purulent), 
557 
purulent,  535 
'  diagnosis  of,  537,  542 

prognosis  of,  538 
symptoms  of,  536,  542 
treatment  of,  538,  544 
with  fistula,  540  Ct, 
without  fistula,  535 
gouty,  658 
grinding  in,  561 
non-septic,  563 

symptomatic,  568 
phagedenic,  650 

septic,  at  bifurcations  of  roots,  561 
symptoms  of,  515 
in  the  temporary  teeth,  557 
traumatic,  563 
causes  of,  563 
diagnosis  of,  566 
pathology  of,  565 
treatment  of,  566 
Pericementum,  blood  supply  to,  175 
calcospherites  in,  180 
degeneration  of,  579,  586,  626 

fibroid  586 
development  of,  154,  158 
fibrosis  of,  586 
fimction  of,  171 
glands  of,  178 
histology  of,  171 
overuse  of,  580 
Periostitis,  maxillary,  544 
proliferative,  134 
suppurative,  134 
Petechia,  111 

Phagedenic  pericementitis,  650 
Phagocytosis,  19,  51 

causes  of,  33 
Phenacetin,  use  of,  362,  443,  671 
Phenol  camphor,  use  of,  372,  441 

sodique,  use  of,  194,  396,  596,  683 
Phosphaturia,  103 
Phosphor  necrosis,  696 
Physical  condition,  abnormal,  28 
Physiology,  morbid,  25 
Pigmentary'  infiltration,  81 
Pigmentation  in  dental  caries,  343 
Pigments  in  tissue,  81 

varieties  of,  81 
Pilocarpine,  oral  effects  of,  568 
Plantation,  mode  of  attachment  in,  577 


714 


INDEX 


Plaster  of  Paris,  use  of,  385 
Plethora,  105 
Podopliyllin,  use  of,  602 
Potassium  bromide,  use  of,  678 
carbonate,  use  of,  369 
chlorate,  use  of,  194,  569,  596 
iodide,  ill  effects  of,  568 
Poultices,  danger  of,  531 
Predisposition  to  disease,  29 
general,  29 
local,  32,  33 
Pregnancy,  dental  pain  from,  677 
Pressure  anesthesia,  442,  447,  452,  458, 
467 
hemorrhage  after,  485 
Prognosis,  definition  of,  25 
Proteid,  composition  of,  18 

fermentation  of,  44 
Protoplasm,  composition  of,  18 

properties  of,  22 
Protozoa  as  disease  causes,  35 
Pseudoodontalgia,  678 
Ptomaines,  44 
Pulp,  abscess  of,  448 
anesthesia  of,  467 
arteriosclerosis  of,  453 
blood  supply  and,  168,  175 
capping  of,  383,  384,  385 
cavity  duplication  of,  243 
constructive  diseases  of,  401 
death  of,  from  impaction,  264 
degeneration  of,  419 
calcific,  419 
cloudy,  462 
colloid,  464 
fatty,  464 
fibroid,  460 
depletion  of,  434,  442,  452 
digestion  of,  494 
exposure  of,  symptoms  of,  383 
gangrene  of,  495 
partial,  502 
histology  of,  164 
'lyperemia  of,  422 
arterial,  422 

devitalization  in,  430 
from  electric  action,  431 
idiopathic,  430 
thermal  toleration  in,  430 
venous,  432 

devitalization  in,  434 
suffusion  in,  433 
infarction  of,  459 
inflaniiiiation  of,  435 

chronic,  452 
jugulation  of,  433 
"knocking  out,"  470 
mummification  of,  492 
neoplasm  of,  465 
nodules,  412 

and  arsenic,  478 
diagnosis  of,  418 
symptoms  of,  416 
puncturing  of,  470 
putrefaction  of,  499 
removal  of,  466,  481 


Pulp,  removal  of,  partial,  491 
sclerosis  of,  452 
suppui-ation  of,  443 
swelling  of,  436 
ulceration  of,  445 
varieties  of,  126 
.    vitality  of,  tests  for,  496 
Pulpitis,  435 
acute,  436 
chronic,  452 

resorption  of  dentine  in,  439 
hyperplastic,  454 
Pus    formation,   stages   of,   in    apical 

abscess,  519 
Putrefaction,  44,  84 
formalin  in,  504 
germs    of,    effects    of    electricity 

upon,  506 
products  of,  499 
of  pulp,  499 
Pyocyaneo-protein,  use  of,  555 
Pyogenic  calculus,  623 
Pyorrhoea  alveolaris,  625 

abscess  secondary  to,  632,  654 
beginning  with  a  marginal  gin- 
givitis, 628 
bridge  and  plates  in,  645 
in  bifurcations  of  roots,  637 
causes  of,  625 
clinical  history  of,  629 
and  dental  caries,  633 
diagnosis  of,  634 
endarteritis  in,  632 
gum  incision  in,  656 
hetroplasty  of  roots  in,  637 
interstitial  gingivitis  in,  630 
and  living  pulps,  633,  636 
looseness  in,  631 
malnutritional  factor  in,  626 
not  dependent  upon  calculus, 

650 
opsonic  index  in,  648 
oral  catarrh  in,  632 
pathology  of,  629 
prevention  of  motion  in,  638 
prophylaxis  in,  635,  649 
recurrence  of,  649 
replantation  in,  644,  648 
splints  for  use  in,  639 
systemic  effects  of,  649 
symptoms  of,  629 
treatment  of,  635 

medicinal,  in,  640 
varieties  of,  628 
Pyrozonc,  use  of,  489,  505,  547,  549,  635 


Quinine,  use  of,  130,  443,  510,  529,  046, 
678 

R 

Rachitis,  101 
Rampart,  maxillary,  151 


INDEX 


715 


Recalcification  of  dentine,  381 
Receptors  of  cells,  23,  54 
Reflex  action,  186,  188 

disorders  of  dental  origin,  666 
of  systemic  origin,  666 
pain,  pathology  of,  671 

from  pericemental  disease,  672 
Refrigeration,  m  apical  irritation,  507 
in  hypersensitive  dentine,  364 
use  of,  528 
Regeneration  of  bone,  137 

of  tissue,  130 
Replantation,  secondary  dentine  after, 

409 
Resorbeut  organ,  205 
Resorption  of  bone,  135,  130 
varieties  of,  601 
of  permanent  roots,  574 
causes  of,  575 
diagnosis  of,  578 
pathology  of,  576 
symptoms  of,  578 
treatment  of,  579 
of  roots  from  impaction,  265 
Retzius,  stripes  of,  in  enamel,  220 
Rheumatism,  99 

contrasted  with  gout,  99 
muscular,  101 
Ridge,  dental,  151 
Robinson's  remedy,  use  of,  369,  370 
Root,  amputation  of,  389,  548 

calcification  of,  158,  161,  162,  164 
canal,  accidents  in  opening,  489 
filling  of,  485 
infection  of,  489 
loss  of  continuitj^  of,  508 
development  of,  157,  158 
drier,  Evans',  use  of,  470 
filling,  immediate,  507 
implantation,  550 
intubation,  513 
malformations  of,  245 
multiple,  246 
perforation  of,  490 
permanent,  formation  of,  208 
resorption  of,  574 
causes  of,  575 
diagnosis  of,  578 
pathology  of,  570 
symptoms  of,  578 
treatment  of,  579 
replantation  of,  549 
resorption  of,  161,  409 
of  permanent,  265 
sterilization  of,  immediate,  504,  505 
transplantation  of,  549 
Rose  geranium,  oil  of,  use  of,  040 


Saccharin,  use  of,  195,  595 
Saccharomyces     albicans     as     disease 

cause,  680 
Salicylic  acid,  use  of,  595 
Saliva,  analysis  of,  609 


Saliva  in  general  malnutrition,  88,  89 
increased  flow  of,  186 
infective  bacteria  in,  682 
non-germicidal  action  of,  49 
Salivary  calculus,  606 

foreign  bodies  in,  610 

hardening  of,  613 

mode  of  deposit  of,  612,  014 

formation  of,  611 
origin  of,  607 
pathological  effects  of,  014 
prognosis  of,  615 
recurrence  of,  607,  620 
scalers  for,  616,  622 
structure  of,  610 
treatment  of,  615 
varieties  of,  607 
Salol,  use  of,  130,  195,  529 
Salter,  lines  of,  in  dentine,  104 
Sanguinary  calculus,  023 
Sapremia,  140 

Saprophytic  bacteria,  41,  44 
Schizomycetes,  38 
Schreger,  lines  of,  in  dentine,  164 

in  enamel,  164,  225 
Sclerosis  of  pulp,  452 
Scorbutus,  101 
Scurvy,  101 

infantile,  202 
oral  effects  of,  568 
Sedation,  results  of,  21 
Sedatives,  use  of,  419,  428,  441,  443,  447, 

452,  484 
Seidlitz  powder,  use  of,  602 
Sepsis,  dental,  398 

general,  of  dental  origin,  093 
intoxication  from,  139 
oral  effects  of,  398 
Septic  intoxication,  127 
Septicemia,  45,  140 

diet  in,  142 
Serres,  glands  of,  178 
Sheaths  of  Neuman,  154 
Silver,  Credo's  ointment,  use  of,  142 
soluble,  use  of,  142 
lactate,  use  of,  647 
nitrate,  use  of,  368,  370,  371,  390, 
391,  392,  398 
Skiagraphy,  use  of,  547,  673 
Skin  eruptions  in  dentition,  194 
Slough,  83,  84 
Sodiiun  biborate,  use  of,  595,  596 

bicarbonate,  use  of,  370,  380,  397, 

678 
chloride,  use  of,  596 
dioxide,  danger  of,  505 

use  of,  303,  369,  410,  489,  505, 
511 
sulphate,  use  of,  113 
Somnoform,  use  of,  418 
Sphacelus,  83,  84 
Sponge  grafting,  use  of,  486 
Stains,  metallic,  296,  300 

non-metallic,  298 
Starvation  of  tissue,  90 
Stellate,  reticulum,  153 


716 


INDEX 


Steresol,  use  of,  267 
Sterilization,  dental,  698 
Stimulation,  effects  of,  59 

results  of,  21 
Staples,  use  of,  562 
Stomach,  blastomycetes  in,  49 
Stomatitis,  682 

classification  of  varieties,  683 

in  dentition,  194 

infective  catarrhal,  683 

mercurial,  684 

beneficial   effects   of   mercury 
in,  568 

simple  catarrhal,  683 

symptomatic  catarrhal,  684 

ulcerosa,  593 

ulcerative,  685 
Strabismus  in  dentition,  191 
Stratum  intermedium,  153 
Subgingival  calculus,  620 
causes  of,  620 
effects  of,  621 
removal  of,  623 
scalers  for,  622 
sjTiiptoms  of,  621 
treatment  of,  623 
Suffusion,  111 

from  arsenic,  481 
Sugar  in  diabetes,  93 

as  source  of  energy,  23,  91 
Sulphur  carbolate,  use  of,  647 

powdered,  use  of,  647 
Sulphuric  acid,  use  of,  113, 469, 483, 489, 

510,  512,  547,  647 
Supernumerary  teeth,  252 
Supplemental  cusps,  244,  245 
Suppuration  in  inflammation,  125 

of  pulp,  443 
Suprarenal  extract,  use  of,  113 
Susceptibility  to  disease,  29 
Symptoms,  definition  of,  25 

objective,  25 

subjective,  25 
Synostosis,  dental,  573 
Syphilis,  dental  pain  from,  677 

of  mouth,  688,  695,  703 

necrosis  of  bone  from,  556 

oral  effects  of,  568 
Syphilitic  teeth,  227,  237 


Talcum  powder,  use  of,  194 
Tannin,  use  of,  370,  484,  495 
Tartar,  cream  of,  use  of,  646 
Teeth,  abrasion  of,  270 
absence  of,  250 
accidents  to,  588 
anomalies  of,  249 
attachment  of,  589 
brushing?  of,  395 
change  in  color  of,  269 
concrescence  of,  241 
conical,  234 
crypts  of,  relations  of,  161 


Teeth,  decalcification  of,  64,  88 

in  dermoid  cysts,  63 

development  of,  151 

disuse  of,  583 

dwarfism  of,  232 

erosion  of,  282 

eruption  of,  causes  of,  181 

flexion  of,  242 

fractures  of,  291 

fusion  of,  237 

gemination  of,  242 

giantism  of,  232 

histology  of,  162 

Hutchinson's  235 

impaction  of,  256 

injury  of  mechanical,  269,  291 

joining  of,  378 

luxation  of,  588 

malformations  of,  222 

malocclusion  of,  581 

malposition  of,  254 

occlusal,  levels  of,  210 

overuse  of,  580 

permanent,  development  of,  160 
eruption  of,  204 

size  of,  variations  in,  232 

structure  of,  in  dental  caries,  317 

supernumerary,  252 

syphilitic,  227,  237 

temporary,  eruption  of,  183 
pericementitis  in,  557 
resorption  of  roots  of,  204 
retained,  208 
Temperament,  classes  of,  31 
Temporary  stopping,  use  of,  557 
Tests  for  hyperemia,  427 

for  pulp  vitality,  496 
Therapeutics,  basis  of,  20 

definition  of,  17,  25 

empirical,  26 

rational,  26 
Thrombosis,  109 
Thymol,  use  of,  385,  422,  441,  447,  452, 

459, 488,  492,  596 
Thymophen,  use  of,  441 
Tissue,  composition  of,  22 

effect  of  acidity  upon,  58,  94,  95 

excessive  destruction  of,  91 

food  supply  to,  22 

regeneration  of,  130 

starvation  of,  90 

waste,  excessive,  138 
Tomes,  granular  layer  of,  158 
Toxalbumins,  44 
Toxaemia,  45,  92,  139 

in  general  malnutrition,  90 
Toxins,  chemotactic  properties  of,  51 

as  ferments,  44 

immunity  to,  55 
Toxoid,  56 
Toxone,  56 

Transplantation,  use  of,  388 
Trephine,  use  of,  529 
Trichloracetic  acid,  use  of,  554,  597,  635, 

646 
Tricresol,  use  of,  503,  561 


INDEX 


717 


Trioxymethelene,  use  of,  371 
Trophic  disturbance,  28,  82 

from  dental  disease,  677 
Tube  casts  in  dental  caries,  340 
Tuberculosis  of  mouth,  692 
Tubes  of  dentine,  164 

of  enamel,  164,  166 
Tubules,  dentinal,  calcification  of,  403 
Tumors,  70 

causes  of,  65 

classes  of,  64,  67 

definition  of,  64 

epithelial,  70 

malignant,  64,  67 

metastasis  in,  71 


U 

Ulceration,  128 

of  pulp,  445 
Uremia,  93 
Urates  in  pericementum,  659 

in  tissue,  95 
Uric  acid  in  gout,  94 
Uvula,  bifid,  150 


Vapocain,  use  of,  364 

Vascular  system,  disturbances  of,  105 

Varnish,  use  of,  369,  377,  442 


Vaseline,  use  of,  678 
Vasomotor  nerves,  114 
Vegetable  fungi,  35,  36 
Veratrine,  use  of,  219 


W 

Waste  removal,  abnormal,  28 
Water,  drinking,  use  of,  603 
Wax,  use  of,  485,  487 
Wood  points,  use  of,  505 


X-iiAY,  use  of,  418,  497,  647,  678 


Zinc  chloride,  use  of,  368,  546,  595,  646 
oxide  and  eugenol,  use  of,  556 

use  of,  194,  381,  385,  428,  488, 
492 
oxvchloride  of,  use  of,  381, 385, 485, 

487,  490,  495,  562 
oxysulphate,  use  of,  385 
phosphate,  use  of,  377,  379,  391, 

428, 476, 503 
sulphate,  use  of,  367 
Zooglea  of  bacteria,  40 


■'•^■:''^i^. 


m 


iWii 


COLUMBIA  UNIVERSITY 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing, 
as  provided  by  the  rules  of  the  Library  or  by  special  ar- 
rangement with  the  Librarian  in  charge. 


C28'r,3e)M60 


RK301 
Burchard 


B892 
1908 


COLUMBIA  UNIVERSITY  LIBRARIES  its  .sL 

RK  301  6892  1908  C.I 

A  text  book  of  dental  pattiology  and  ther 


2002339137 


